The role of light in shaping plant growth: mechanisms of photomorphogenesis and hormonal integration during seedling development

Introduction

Plants utilize light as both a primary energy source and a high-fidelity environmental signal that orchestrates nearly every phase of their life cycle. From the initiation of germination to the establishment of photosynthetic competence, light serves as a master regulator, integrating external cues with endogenous developmental programs. Unlike mobile organisms, plants exhibit remarkable developmental plasticity, continuously reshaping their morphology to optimize light capture (Huq et al., 2024). This adaptability is governed by a sophisticated sensory network of photoreceptors and downstream signaling cascades that precisely synchronize gene expression, metabolic flux, and cellular differentiation in response to the ambient light environment (Paik and Huq, 2019).

The transition from skotomorphogenesis to photomorphogenesis

The first step in the development of a new plant is seed germination. Following this event, seedlings undergo a dramatic developmental transition dictated entirely by light availability. This transition represents an acute ecological bottleneck and an absolute determinant of survival. In nature, a seed germinating beneath the soil surface has access to a strictly finite reservoir of endosperm or cotyledonary storage reserves. In the absence of light, seedlings commit to a subterranean survival strategy known as skotomorphogenesis (etiolation). This program is characterized by rapid hypocotyl elongation, the maintenance of a protective apical hook, tightly closed cotyledons, and the development of etioplasts rather than functional chloroplasts. This highly specialized growth is a high-stakes evolutionary gamble, where all available metabolic energy is diverted exclusively into upward vertical extension to penetrate the soil surface as fast as possible, while shielding the sensitive shoot apical meristem from mechanical damage (Howe, 2024). If this dark state persists too long and the seedling fails to breach the soil, it exhausts its carbon reserves, leading to irreversible starvation, collapse, and death. Light, therefore, acts as an indispensable lifeline and a developmental rescue signal. Upon exposure to light at the soil surface, the seedling immediately switches to photomorphogenesis (de-etiolation). This program triggers a fundamental, whole-plant reprogramming: hypocotyl elongation is rapidly arrested, cotyledons expand and open, and chloroplast biogenesis is activated to jumpstart photosynthesis (Howe, 2024). By shifting the plant from a vulnerable, heterotrophic reliance on maternal seed reserves to self-sustaining, autotrophic growth, this light-triggered switch successfully secures the seedling’s establishment in its environment (Huq et al., 2024).

Photoreceptor networks and core signaling hub

Plant developmental plasticity relies on a sophisticated photoreceptor network that monitors specific regions of the light spectrum. Phytochromes (PHYA-PHYE) serves as the primary sensors for the red (R) and far-red (FR) light, while cryptochromes (CRY1, CRY2) and phototropins (PHOT1, PHOT2) absorb blue and UV-A wavelengths. Additionally, the Zeitlupe family (ZTL, FKF1, and LKP2) functions as specialized blue-light sensors, and UV RESISTANCE LOCUS 8 (UVR8) acts as the primary sensor for UV-B light (Lin, 2002; Burgie and Vierstra, 2014; Huq et al., 2024). These photoreceptors operate as molecular switches through light-driven conformational changes. For instance, light converts inactive Pr phytochromes into the active Pfr form, which translocates to the nucleus to trigger signaling (Al-Sady et al., 2006; Bae GabYong and Choi Giltsu, 2008; Jung et al., 2016). Similarly, nuclear cryptochromes interact with transcription factors like CIB to drive light responses, while membrane-associated phototropins undergo autophosphorylation to guide phototropism and stomatal opening (Okajima, 2016; Wang et al., 2016).

The transition to photomorphogenesis is ultimately achieved by deactivating two primary repressive modules, the CONSTITUTIVELY PHOTOMORPHOGENIC 1/SUPPRESSOR OF PHYA-105 (COP1/SPA) complex and PHYTOCHROME-INTERACTING FACTORs (PIFs) (Sullivan et al., 2003). The COP1/SPA complex is a central E3 ubiquitin ligase that maintains skotomorphogenesis in darkness by targeting positive regulators, such as the master transcription factor ELONGATED HYPOCOTYL 5 (HY5), for proteasomal degradation (Lau and Deng, 2010; Hoecker, 2017). It also regulates the abundance of photoreceptors themselves, providing a vital feedback mechanism to reset light responses (Weidler et al., 2012). This dual role demonstrates that the complex does not merely repress light signaling in the dark; it also provides a vital feedback mechanism to attenuate and reset photoreceptor responses under illuminated conditions. Upon light perception, activated photoreceptors (e.g., Pfr or activated CRY) physically interact with the COP1/SPA complex within the nucleus. This interaction triggers either the nuclear export of COP1 or the biochemical disruption of the complex’s activity. This inactivation allows HY5 and other positive regulators to accumulate, initiating the transcriptional programs that drive photomorphogenesis. Parallel to this, PIFs accumulate in the nucleus during darkness to activate elongation growth (Martin et al., 2016). Hence the two modules work simultaneously; upon light perception, activated photoreceptors physically interact with these repressors, triggering the nuclear export or inactivation of COP1 and the rapid phosphorylation and degradation of PIFs (Cai and Huq, 2025). This coordinated relief of repression allows HY5 and other light-responsive genes to accumulate, establishing the COP1-HY5 and PIF modules as the principal branches for integrating environmental and hormonal signals.

Integration of light and phytohormonal network

Light signaling exhibits extensive crosstalk with phytohormonal network to fine-tune growth responses (Bawa et al., 2020; Carrera-Castaño et al., 2020; Miao et al., 2021; Zhao et al., 2022; Yun et al., 2023; Gómez-Ocampo et al., 2024).This integration begins at the earliest stages of the life cycle; for instance, ABA and GA act as the primary master regulators of seed dormancy and germination, with light acting as the switch that shifts the hormonal balance towards germination. During seedling establishment, light typically inhibits hypocotyl elongation by downregulating auxin signaling and decreasing bioactive GA levels (An et al., 2012; Zhao et al., 2022). While GA promotes cell expansion, its levels are tightly restricted under illuminated conditions to prevent excessive growth. Similarly, auxin is essential for establishing growth asymmetry and regulating cell elongation during tropic responses, yet its activity is redirected upon light perception to facilitate de-etiolation (Bawa et al., 2020; Yun et al., 2023). Developmental plasticity is further modulated by BRs, which generally promote etiolated traits, and cytokinins, which work synergistically with light to drive cell differentiation and chloroplast development (Guan et al., 2014; Cortleven et al., 2016; Gómez-Ocampo et al., 2024). Furthermore, ethylene and ABA serve as checkpoints for developmental timing, acting either antagonistically or synergistically with light to regulate apical hook maintenance and stress adaptation (Ali et al., 2022; Zhao et al., 2022). Collectively, this multilayered hormonal crosstalk ensures that plant development remains exceptionally flexible, precisely balancing internal growth programs with fluctuating environmental cues.

Environmental modulation of photomorphogenesis

Photomorphogenesis does not occur in isolation; it is continuously modulated by other vital environmental variables, most notably ambient temperature and canopy shade. In nature, plants perceive a reduction in the R to FR (R/FR) ratio as an indicator of competing neighboring vegetation, triggering the shade avoidance response (SAR). SAR reverses several photomorphogenic traits, accelerating hypocotyl elongation at the expense of leaf and root development (Legris et al., 2019). Similarly, elevated ambient temperatures (thermomorphogenesis) can override light-mediated growth restriction, utilizing shared molecular components like PIF4 to stimulate elongation and alter architecture. This complex interplay ensures that the seedling’s morphological strategy is optimized not just for light presence, but for the realistic, multi-stress dynamics of its natural habitat (Casal and Balasubramanian, 2019).

Coordinated development along the shoot-root axis

Seedling development provides a definitive framework for understanding how light and hormonal signals are integrated across the entire plant body. The successful exit from seed dormancy initiates a cascade of developmental milestones, where the same regulatory nodes that triggered germination are repurposed to guide the seedling’s physical transition into the environment. Aerial processes like hypocotyl arrest and cotyledon expansion are the most visible hallmarks of photomorphogenesis, but light also fundamentally shapes root system architecture. Although roots typically grow in darkness, they perceive light indirectly via systemic signals transmitted from the shoot. This bidirectional communication, involving mobile transcription factors, phytohormones, and sugars, allows the aerial light environment to modulate lateral root formation and nutrient acquisition (Miotto et al., 2021). Notably, research using specialized platforms like the Dark-Root (D-Root) system has revealed that standard laboratory illumination of roots can trigger artificial ROS bursts and disrupt cytokinin homeostasis (Yokawa et al., 2014; Novák et al., 2015). Viewing the seedling through this lens highlights the holistic nature of plant development, where tissues operate as a dynamic, integrated system.

Recent advances in molecular genetics, high-resolution imaging, and systems biology have redefined light signaling as a highly dynamic network rather than a linear pathway (Pradhan et al., 2026). This review dissects the intricate mechanisms governing light-mediated seedling development, focusing specifically on the synergy between sensory perception and hormonal flux. By tracing the developmental arc from germination to the establishment of complex root architecture, we provide a comprehensive synthesis of how plants interpret light as their definitive environmental compass to optimize fitness and survival.

Seed germination

Seed dormancy and germination are highly complex and inter-linked physiological states that determine a plant’s successful entry into the environment (Bewley, 1997; Baskin and Baskin, 2000). Seed dormancy serves as a biological safety-delay, preventing germination even under seemingly optimal conditions to ensure long-term survival. Conversely, germination marks the definitive transition from a quiescent embryo to a metabolically active seedling. This transition is governed by a sophisticated integration of environmental cues such as water, oxygen, temperature, and in some species nutrient availability with internal regulatory networks, including hormonal flux, transcriptional reprogramming, metabolic pathways, and epigenetic modifications (Longo et al., 2020; Sajeev et al., 2024; Li et al., 2026).

Among these external signals, light serves as the master regulator. In many species, such as Arabidopsis thaliana, red light is the fundamental requirement that initiates the germination program. PHYB acts as the primary sensor in this process (Shinomura et al., 1994). Upon the absorption of red light, PHYB undergoes a conformational shift from Pr form to the active Pfr form, which promotes germination. By targeting repressive transcription factors for degradation, the Pfr form effectively releases the brakes on light-regulated development. This molecular reset initiates critical developmental shifts, primarily the transition from seed dormancy to active germination and the subsequent shift from heterotrophic etiolated growth to autotrophic de-etiolation. Conversely, FR light or prolonged darkness triggers the reversion of Pfr back to the inactive Pr form, thereby maintaining dormancy.

Light does not act in isolation, while ABA and GA serve as the master switches, a suite of other hormones and factors fine-tune the germination process (Seo et al., 2009; Lau and Deng, 2010; Shu et al., 2016; Carrera-Castaño et al., 2020; Yang et al., 2020c; Smolikova et al., 2021; Ali et al., 2022; Farooq et al., 2022; Li et al., 2022; Zhao et al., 2022; Sajeev et al., 2024). The decision to germinate is fundamentally a tug-of-war between two antagonistic hormones: ABA, which induces dormancy and represses germination, and GA, which triggers dormancy release and promotes germination (Longo et al., 2020; Gianinetti, 2023). The ABA/GA ratio, rather than absolute hormone levels, dictates the seed’s developmental fate whether it germinates or remains dormant. Light acts as the environmental switch that tilts the balance, favoring GA dominance during germination and shifting towards ABA during dormancy through multiple molecular mechanisms.

The light-labile bHLH transcription factor PIF1 (also known as PIF3-LIKE 5/PIL5) functions as the central hub integrating light signals into these hormonal pathways. In Arabidopsis thaliana, PIF1 is the primary negative regulator of phytochrome-mediated germination (Oh et al., 2004). As mentioned earlier, exposure to red light converts PHYB into its active Pfr form, which facilitates its translocation into the nucleus, where the Pfr form interacts directly with PIF1, inducing phosphorylation and subsequent degradation of PIF1 via the 26S-proteasome pathway (Oh et al., 2006; Li et al., 2011; Cheng et al., 2021). The removal of PIF1 serves as the molecular green light for germination, leading to a surge in GA levels and a concomitant drop in ABA. This shift triggers the degradation of repressor DELLA proteins and the activation of cell wall-remodeling enzymes, allowing the embryo to expand and break through the seed coat. In darkness or FR light, the absence of active Pfr allows PIF1 to accumulate in the nucleus, thereby maintaining high ABA and low GA levels (Oh et al., 2009). PIF1 increases the expression of ABA biosynthetic genes ABSCISIC ACID DEFICIENT (ABA1), NINE-CIS-EPOXYCAROTENOID DIOXYGENASE6 (NCED6) and NCED9 while decreasing the ABA catabolic gene CYP707A2 (Oh et al., 2007, 2009). Furthermore, PIF1 enhances the expression of ABSCISIC ACID-INSENSITIVE 3 (ABI3) and ABI5, the key transcription factor in ABA signaling pathway (Oh et al., 2009). Conversely, PIF1 negatively regulates GA biosynthetic genes GIBBERELLIN 3-OXIDASE 1(GA3ox1) and GA3ox2 and positively regulates the GA catabolic gene GA2ox2 (Oh et al., 2006, 2009). PIF1 also increases the expression of two DELLA genes, GA-INSENSITIVE (GAI) and REPRESSOR OF GA1-3 (RGA/RGA1), thereby inhibiting the GA signaling (Oh et al., 2007).

PIF1 also interacts with other regulators like REVEILLE 1 (RVE1) and RVE2, which are MYB-like transcription factors acting as activators of seed dormancy and inhibitor of PHYB-mediated seed germination (Jiang et al., 2016). RVE1 directly inhibit the transcription of GA anabolic gene GA3ox2 (Jiang et al., 2016). PIF1 and RVE1 promote each other’s DNA-binding ability and transcriptional activity, forming a feedback loop to regulate the expression of ABA- and GA-related genes (Yang et al., 2020a). Furthermore, RVE1 interacts with both the DELLA repressor, REPRESSOR OF GA-LIKE2 (RGL2) and its E3 ubiquitin ligase SLEEPY1 (SLY1), preventing the degradation of RGL2 to maintain dormancy (Yang et al., 2020b). Recent findings suggest that GA receptors (GID1s) and ABA receptors (PYLs), directly compete for binding to RGL2, exerting opposite effects on its stability (Nie et al., 2026). PIF1 also regulates GA/ABA metabolism indirectly, through the induction of nucleus-localized zinc-finger protein SOMNUS (SOM) and the zinc-finger transcription factor DOF AFFECTING GERMINATION 1 (DAG1) (Kim et al., 2008; Gabriele et al., 2010). SOM and DAG1, functioning downstream of the PIF1, maintain seed dormancy by positively regulating ABA while negatively regulating GA metabolism (Kim et al., 2008; Gabriele et al., 2010). DAG1 prevents seed germination by silencing GA biosynthetic gene AtGA3ox1 (Gabriele et al., 2010; Boccaccini et al., 2014). Additionally, PIF1 coordinates with DELAY OF GERMINATION 1 (DOG1), an essential dormancy regulator. In darkness, DOG1 levels remain high, enhancing ABA signaling by promoting ABI5 expression and depressing the activity of the negative regulator PP2C phosphatases (AHG1, AHG3). In light, the loss of PIF1 works in parallel with the decline of DOG1 pathway activity, shifting the ABA/GA ratio to favor germination (Carrillo-Barral et al., 2020). PIF1 inhibits seed germination not only via ABA and GA, but also by coordinating various hormone signaling pathways and by modulating cell wall remodeling genes, including EXPANSINS (EXP) and XYLOGLUCAN ENDOTRANSGLUCOSYLASE/HYDROLASE (XTH) (Oh et al., 2009). This multi-layered interplay coordinating light perception, core transcription factors, antagonistic hormone flux, and cell wall modifications is comprehensively modelled in Figure 1.

Recent research has significantly expanded our mechanistic understanding of seed dormancy and germination beyond traditional transcriptional and translational regulation (Sajeev et al., 2024). Increasing evidence highlights the involvement of multilayered epigenetic regulation incorporating DNA methylation, histone modification, chromatin remodeling, small RNA and long non-coding RNA mediated mechanisms (Wang et al., 2022a, 2023; Chow and Mosher, 2023; Sajeev et al., 2024). These epigenetic processes act both as stabilizers of developmental memory and as dynamic regulators permitting rapid response to light cues. Together, they form an integrated regulatory framework that ensures germination proceeds only under favorable conditions.

Hypocotyl development

Hypocotyl elongation is a critical developmental strategy that enables the seedling to reach light post-germination. This process is governed by a precise interplay between light quality and a dynamic phytohormone landscape. High R/FR ratios and blue light inhibit hypocotyl elongation primarily through PHYB and CRY1 signaling. These photoreceptors converge on the COP1-HY5-PIF regulatory hub to repress growth once the seedling emerges from the soil (Gómez-Ocampo et al., 2024).

The canonical COP1-HY5 pathway remains the central engine of hypocotyl regulation. In darkness or low-quality light, the E3 ligase COP1 translocates to the nucleus to ubiquitinate the transcription factor HY5, targeting it for degradation. The resulting loss of HY5 relieves the repression of elongation and indirectly amplifies PIF4-mediated growth. Recent structural insights by Malakar et al., 2025 identified that a specific W467 mutation in COP1 compromises its ability to degrade HY5, leading to constitutive HY5 accumulation and suppressed hypocotyl growth even in total darkness. Conversely, HY5 acts as a multidimensional growth brake under high light or UV-B stress by coordinating several hormonal pathways. It actively suppresses GA biosynthesis while simultaneously stabilizing DELLA proteins, the primary repressors of cell expansion (Miao et al., 2021). Furthermore, HY5 enhances the kinase activity of BRASSINOSTEROID-INSENSITIVE 2 (BIN2), a negative regulator of BR signaling, to further restrict growth (Li et al., 2020). Beyond the HY5-mediated brake, recent findings highlight the role of B-box proteins in growth suppression. B-Box-containing zinc finger 21 (BBX21), an essential component of light-mediated development, has been shown to inhibit hypocotyl elongation by forming a regulatory module with BRASSINAZOLE-RESISTANT 1 (BZR1) and PIF4 (Gómez-Ocampo et al., 2024). In this BBX21-BZR1–PIF4 cascade, BBX21 acts as a light-dependent scaffold or co-regulator that prevents PIF4 from promoting elongation, thereby reinforcing the transition to photomorphogenesis. This coordination is further refined by SUPPRESSOR OF MAX2 1 (SMAX1), which links the GA-DELLA pathway with karrikin signaling to fine-tune developmental responses (Kim et al., 2022).

Recent studies have uncovered sophisticated layers of circadian and epigenetic control over hypocotyl growth. Components of the circadian Evening Complex (EC), specifically EARLY FLOWERING 3 (ELF3) and LUX ARRHYTHMO (LUX), inhibit phototropic bending and hypocotyl elongation in light-grown seedlings by acting as gatekeepers upstream of PIF4 and PIF5 (Cobb et al., 2025). The HISTONE DEACETYLASE 1 COMPLEX (HDC1) stimulates growth under red light by stabilizing the PIF4 protein and deacetylating specific red-light-induced genes, providing a dual layer of chromatin-level control (Wang et al., 2022a). The temperature-regulated H2A.Z-PIF4 pathway enhances growth during heat stress. Elevated temperatures trigger the eviction of H2A.Z histones from the PIF4 promoter, facilitating its transcriptional activation and subsequent auxin-mediated elongation to optimize light capture and enhance evaporative cooling (Verma et al., 2024). This response is mirrored in crops for instance, under low light and high temperature, soybean seedlings exhibit a surge in GA₃, GA₇, and indole-3-acetic acid (IAA) via the upregulation of GmGA3ox1/2 and GmYUCCA3/5/7 (Bawa et al., 2020). Such findings highlight a conserved hormonal crosstalk strategy used by plants to drive cell expansion under multi-environmental stress.

The final physical manifestation of elongation is dictated by rapid changes in cell wall architecture, often regulated by non-coding RNAs. The miR775-GALACTOSYLTRANSFERASE 9 (GALT9) cascade provides a rapid mechanism to halt elongation during the dark-to-light transition. HY5 repression leads to the accumulation of GALT9 in transverse cell walls, which hardens the wall through pectin accumulation and cross linking (Zhang et al., 2025). Additionally, miR160 regulates auxin-dependent growth by inhibiting AUXIN RESPONSE FACTOR (ARF) 10/16/17 (Dai et al., 2021). This is critical because auxin exhibits a bifunctional nature; while low concentrations stimulate growth, high concentrations can inhibit it by altering apoplastic pH balance and cell wall extensibility (Wang et al., 2025). Long non-coding RNAs (lncRNAs) like BoNR8 and AtR8 function as molecular connectors between light and ABA signals, modulating the activity of PIF4 and ABI3 to produce opposing growth responses based on environmental stress levels (Zhang et al., 2023). Through this integrated framework, the seedling ensures that its growth is perfectly synchronized with its environment, maximizing light capture while minimizing energy waste and stress vulnerability.

Apical hook formation and maintenance

The apical hook is a crucial morphological adaptation during the early germination of dicotyledonous seedlings. It acts as a protective structure of the shoot apical meristem and cotyledons as the seedling pushes and comes out through the soil (Wang and Guo, 2019). This transient structure ensures that delicate tissues are not damaged during emergence. Apical hook development proceeds through three distinct phases of formation, maintenance, and opening. The three phases are tightly regulated by hormonal and environmental cues (Silk and Erickson, 1978; Raz and Ecker, 1999).

The asymmetric distribution of auxin plays a central role in the process. It drives differential cell elongation between the inner and outer sides of the hook. During the formation phase, growth is suppressed on the inner side while the outer side elongates, producing the apical hook curvature in a germinating seedling. Reporter studies done using DR5::GUS and DR5::GFP lines revealed auxin accumulation on the inner side of the hook (Friml et al., 2002; Benková et al., 2003; Žádníková et al., 2010). This auxin maximum is established by coordinated activity of transporters, including the efflux carriers (PIN-FORMED 1/PIN1, PIN3, PIN4, and PIN7) and the influx carriers AUXIN RESISTANT 1 (AUX1) and LIKE AUX1 (LAX1) (Vandenbussche et al., 2010; Žádníková et al., 2010, 2016; Wang and Guo, 2019). Auxin activates multiple downstream signaling components namely SMALL AUXIN UP-RNA (SAUR), GRETCHEN HAGEN 3 (GH3), AUXIN/INDOLE-3-ACETIC ACID (AUX/IAA), and ARF (Žádníková et al., 2010, 2016; Wang and Guo, 2019). High auxin levels on the inner side lead to the repression of cell wall expansion. Specifically, high levels of SAURs inhibit PROTEIN PHOSPHATASE 2C CLADE D (PP2C.D) phosphatases. When PP2C.D is inactivated, ARABIDOPSIS H+-ATPase2 (AHA2) proton pumps remain dephosphorylated and inactive. The inactivation of AHA2 prevents the acidification required for cell wall loosening (Spartz et al., 2014; Ren et al., 2018). Cortical microtubules and cell wall-modifying enzymes further reinforce auxin asymmetry, stabilizing hook curvature (Jewaria et al., 2021).

Ethylene also plays a central role in apical hook development, particularly in the maintenance phase. Etiolated (dark-grown) seedlings display the classic triple response, inhibition of stem elongation, radial swelling, and apical hook formation. Ethylene helps maintain curvature by promoting cell division on the inner side of the hook (Vandenbussche et al., 2010). It escalates auxin biosynthesis through the activation of TRYPTOPHAN AMINOTRANSFERASE RELATED 2 (TAR2) gene and increases the abundance of PINs, AUX1, and PIN3/7 transporters; however, the possibility of direct induction of auxin biosynthesis genes is yet to resolved. It also reduces ARF2 protein levels, a negative regulator of auxin signaling. Ethylene hence sustains auxin maxima and ensures maintenance of apical hook (Guo and Ecker, 2003; Potuschak et al., 2003; Vandenbussche et al., 2010; Žádníková et al., 2010).

HOOKLESS 1 (HLS1) is a key regulator of apical hook development, acting downstream of ethylene. Loss-of-function hls1 mutants show complete ethylene insensitivity in hook curvature (Li et al., 2004). Ethylene induces HLS1 protein accumulation, and its transcription is directly regulated by transcription factors ETHYLENE INSENSITIVE 3 (EIN3) and ETHYLENE INSENSITIVE 3-LIKE 1 (EIN3/EIL1) (Lehman et al., 1996; Li et al., 2004; An et al., 2012; Wang and Guo, 2019). These factors also mediate the effects of GA and JA through DELLA-EIN3 and MYC2-EIN3 interactions (An et al., 2012; Song et al., 2014; Zhang et al., 2014, 2018). PIFs further activate HLS1 gene transcription, forming a transcriptional couple with EIN3/EIL1 that integrates hormonal and environmental signals (Gallego‐Bartolomé et al., 2011; An et al., 2012; Zhang et al., 2014, 2018; Jeong et al., 2016; Shen et al., 2016; Shi et al., 2018). Despite its essential role in apical hook development, HLS1’s biochemical function remains unresolved. Sequence homology suggests it may act as an N-acetyltransferase, supported by reduced histone H3 acetylation at WRKY DNA-BINDING PROTEIN 33 (WRKY33) and ABI5 loci in hls1 mutants (Lehman et al., 1996; Li et al., 2004; Liao et al., 2016). However, direct enzymatic activity has not been demonstrated, leaving its mechanistic role enigmatic.

GAs also contributes to both formation and maintenance phases via HLS1 and also by regulating cell elongation and division on the outer side of the hook (Vriezen et al., 2004; Gallego‐Bartolomé et al., 2011; An et al., 2012; Mazzella et al., 2014). They control the expression of WAVY ROOT GROWTH 2 (WAG2 kinase), an auxin transport regulatory protein expressed in a GA-dependent manner on the inner side. WAG2 phosphorylates PIN proteins to fine-tune auxin transport. GAs also interacts with PIFs directly and via WAG2 kinase (Willige et al., 2012). Furthermore, GA signaling promotes degradation of DELLA proteins, which otherwise bind EIN3/EIL1 and inhibit ethylene signaling. By removing DELLA repression, GAs facilitate EIN3/EIL1 activity, reinforcing ethylene-auxin crosstalk (An et al., 2012; Mazzella et al., 2014).

BRs also promote hook formation through extensive hormonal crosstalk. The BIN2 kinase links BR signaling with auxin by phosphorylating ARF2, reducing its activity and enhancing auxin-responsive gene expression (Vert et al., 2008). BZR1 interacts with EIN3 and PIFs, which directly regulate HLS1 (Zhao et al., 2021; Wang et al., 2023). BRs additionally increase GA synthesis, which leads to the degradation of DELLAs that would otherwise inhibit BZR1 (Zhao et al., 2021; Wang et al., 2023). This multilayered interaction highlights how BRs integrate with auxin, ethylene, and GAs to coordinate hook development.

Upon exposure to light, the apical hook undergoes opening, marking the transition to photomorphogenesis. Photoreceptors such as PHYA, PHYB, and CRY1 are activated (Liscum and Hangarter, 1993a, b), leading to repression of COP1. Activated phytochromes also inhibit PIF proteins and disrupt the auxin gradient (Leivar and Quail, 2011; Lau and Deng, 2012). Low PIF3 increase the expression of the BBX23, a transcription factor and repressor of photomorphogenesis, and elevate PP2C levels, ultimately promoting hook opening (Sentandreu et al., 2011). Light lowers the GA levels and also affects the auxin transporter ATP-BINDING CASSETTE B19 (ABCB19), which is primarily localized on the inner side of the apical hook (Ait-Ali et al., 1999; Achard et al., 2007; Alabadí et al., 2008; Wu et al., 2010). Apical hook development exemplifies the intricate interplay between hormonal and environmental signals. Auxin establishes the fundamental asymmetry, while ethylene, GAs, BRs, and HLS1 integrate multiple pathways to sustain curvature until light exposure reprograms these networks to trigger hook opening and seedling establishment. The major molecular players involved in apical hook development and maintenance are indicated in Figure 2.

Cotyledon opening

Cotyledon opening marks a critical developmental shift where a germinating seedling transitions from skotomorphogenesis to photomorphogenesis. This process involves the unrolling and expansion of embryonic leaves to initiate photosynthesis. It is a tightly orchestrated event, governed by an intricate network of light signals, hormonal crosstalk, and transcriptional regulation. The central on/off switch for this transition is the antagonistic relationship between COP1 and HY5. In darkness, the active COP1-SPA1 complex functions as an E3 ubiquitin ligase, targeting photomorphogenesis-promoting transcription factors like HY5 for degradation, thereby keeping cotyledons closed. Light signals inactivate COP1, allowing HY5 to accumulate. As a transcriptional master switch, HY5 activates genes required for expansion and chloroplast development while simultaneously repressing genes that maintain the closed state (Zheng et al., 2017).

JA is a vital positive regulator of the dark-to-light transition. It promotes opening by inhibiting COP1 activity via the CORONATINE INSENSITIVE 1-JASMONATE ZIM DOMAIN-MYC2 (COI1-JAZ-MYC2) pathway. Specifically, JA disrupts the COP1-SPA1 complex, which stabilizes HY5 and other transcription factors such as PHYTOCHROME RAPIDLY REGULATED 1 (PAR1), and PAR2. By suppressing the primary repressor COP1, JA allows light-responsive genes to prime for activation even before the seedling reaches full light exposure. The failure of coi1 or myc2 mutants to open properly demonstrates JA’s essential role in integrating hormonal status with the plant’s light-sensing machinery (Zheng et al., 2017).

While JA pushes for opening, other signals like BR, ABA and melatonin act as brakes to maintain closure until conditions are optimal. The BR-regulated transcription factor BZR1 promotes closure in the dark. HY5 and BZR1 physically interact to provide a check-and-balance system; light-activated HY5 suppresses BZR1, while dark-activated BZR1 maintains closure and hypocotyl elongation (Li and He, 2016). BBX32 works alongside BZR1 to activate closure-related genes like WAG2 and LAX3, which actively maintain the closed state (Favero, 2021; Ravindran et al., 2021, 2025). ABA serves as a post-transcriptional regulator. Light-induced reductions in ABA alter the activity of splicing factors, such as SERINE/ARGININE-RICH (SR) and U2 AUXILIARY FACTOR (U2AF) proteins. This alternative splicing shift enables the proper expression of genes required for cotyledon expansion (Martín et al., 2025). Melatonin acts to delay unfolding. HY5 promotes cotyledon opening by repressing SEROTONIN N-ACETYLTRANSFERASE 6 (AtSNAT6), thereby lowering melatonin levels in the light. Conversely, in the dark, COP1-mediated degradation of HY5 allows melatonin levels to rise, delaying cotyledon unfolding (Wang et al., 2022b).

The physical expansion of the cotyledons requires the coordination of cell wall loosening and the maturation of chloroplast. The transcription factors TEOSINTE BRANCHED 1/CYCLOIDEA/PROLIFERATING CELL FACTOR 15 (TCP15) and GOLDEN2-LIKE 1 (GLK1) are central to this coordination. Upon light exposure, they activate auxin-responsive SAUR genes (e.g., SAUR6, 14, 50, 51) and cell wall-loosening genes like EXPB1 and EXPB3. Simultaneously, they support chloroplast formation by upregulating chlorophyll-binding genes (e.g., LIGHT-HARVESTING CHLOROPHYLL B-BINDING 1.4/LHCB1.4), ensuring the leaf is functionally ready to photosynthesize as it expands (Alem et al., 2022). TCP10 plays a similar role, ensuring efficient unfolding by coordinating hormonal and photosynthetic gene expression (Alem et al., 2025). The SAUR family provides a molecular switch for this process. In darkness, SAUR17 binds and protects PROTEIN PHOSPHATASE 2C CLADE D1 (PP2C-D1) to maintain closure. Light-induced SAUR50 inhibits PP2C-D1, triggering the cell expansion necessary for opening (Wang et al., 2020). The dark to light transition is ultimately governed by phytochromes and PIFs. In darkness, PIF3 suppresses TCP4 to prevent expansion. Upon light exposure, the degradation of PIF3 releases TCP4 to activate expansion genes SAUR16 and SAUR50 (Dong et al., 2019). The transition is refined by specific light spectra. Activated by FR light via PHYA, the transcription factor ARABIDOPSIS THALIANA ACTIVATING FACTOR 1 (ATAF1) works with HY5 to inhibit closure-related genes such as 1-AMINOCYCLOPROPANE-1-CARBOXYLATE SYNTHASE 5 (ACS5), PIN3, and BBX32 (Yao et al., 2024). Finally, internal signals ensure the seedling is ready for light. GENOMES UNCOUPLED 1 (GUN1)-mediated plastid signaling acts as a fail-safe. If chloroplasts are under stress or not yet functional, GUN1 can inhibit light-driven expansion. This ensures that cotyledon opening is perfectly synchronized with the functional state of the photosynthetic machinery (Veciana et al., 2025). Key molecular regulators contributing to light mediated Cotyledon opening are depicted in Figure 3.

Greening and chloroplast biogenesis

The greening of germinating seedlings marks a critical developmental transition from heterotrophic to photoautotrophic growth, characterized by the conversion of colorless proplastids into functional chloroplasts and the activation of photosynthesis. This coordinated process involves pigment biosynthesis and the activation of photosynthetic machinery, ensuring the seedling shifts from utilizing stored seed reserves to performing autotrophic metabolism powered by light. It begins with seed imbibition, which reactivates metabolism, mobilizes stored reserves, and initiates transcription in both the nucleus and plastids. In the cotyledons, undifferentiated plastids start to develop into chloroplasts, while in roots they form amyloplasts (Nakabayashi et al., 2005; Bassel et al., 2008; Howell et al., 2009). Plastid gene transcription is mediated by two nuclear-encoded RNA polymerases, RPOTp and RPOTmp (collectively NEP), and a plastid-encoded RNA polymerase (PEP) (Courtois et al., 2007; Liere et al., 2011). Early in germination, NEP transcribes housekeeping genes, but as light exposure increases, PEP becomes active and drives expression of photosynthetic genes encoding components of Photosystem I (PSI), Photosystem II (PSII), RIBULOSE-1,5-BISPHOSPHATE CARBOXYLASE/OXYGENASE (RuBisCO), and light-harvesting complexes (Demarsy et al., 2006; Zhelyazkova et al., 2012). This NEP-to-PEP transition represents the first major transcriptional hallmark of plastid biogenesis.

In darkness, the seedling follows the skotomorphogenic program its hypocotyl elongates, cotyledons remain folded, and proplastids differentiate into etioplasts containing prolamellar bodies that store protochlorophyllide (Pchlide) bound to NADPH-PROTOCHLOROPHYLLIDE OXIDOREDUCTASE (POR) (Mansfield and Briarty, 1991). This configuration maintains the potential for chlorophyll synthesis but halts the process in the absence of light. Upon illumination, light perception by phytochromes (PHYA, PHYB) and cryptochromes (CRY1, CRY2) triggers the photomorphogenic switch (Quail, 2002). Light-activated phytochromes convert from the Pr to Pfr form, translocate to the nucleus, and promote the degradation of PIF1, PIF3, PIF4, and PIF5, which normally repress chlorophyll biosynthetic and photosynthetic genes such as GLUTAMYL-TRNA REDUCTASE 1 (HEMA1), MAGNESIUM CHELATASE H SUBUNIT (CHLH), GUN5 and PORC (Moon et al., 2008; Shin et al., 2009). Their removal lifts repression, allowing expression of genes required for greening. Concurrently, light inhibits the activity of the COP1/DE-ETIOLATED 1 (DET1) E3 ubiquitin ligase complex, stabilizing the transcription factor HY5, which binds to G-box motifs in the promoters of photosynthesis-associated nuclear genes (PhANGs) and activates chlorophyll biosynthetic enzymes such as HEMA1, CHLH, GUN4, CHLOROPHYLLIDE A OXYGENASE (CAO), and PORA/B/C (Lee et al., 2007).

The first biochemical step of greening occurs when POR catalyzes the photoreduction of Protochlorophyllide (Pchlide) to chlorophyllide, which is subsequently converted into chlorophyll a and b (Beale and Castelfranco, 1973; Tanaka and Tanaka, 2007). This triggers the disassembly of prolamellar bodies, thylakoid membrane formation, and photosystem assembly (Privat et al., 2003; Reinbothe et al., 2010). Simultaneously, transcriptional regulators such as the Golden2-like factors GLK1 and GLK2 promote photosystem and light-harvesting gene expression (Waters et al., 2009), while cytokinin-induced GATA factors NITRATE-INDUCIBLE, CARBON-METABOLISM INVOLVED (GNC) and CYTOKININ-RESPONSIVE GATA1 (CGA1) enhance chloroplast differentiation and chlorophyll accumulation (Hudson et al., 2011; Chiang et al., 2012). The APETALA 2/ETHYLENE RESPONSIVE FACTOR (AP2/ERF)-family factor CYTOKININ RESPONSE FACTOR 2 (CRF2) also supports chloroplast division through activation of PLASTID DIVISION 2 (PDV2) (Okazaki et al., 2009). Together, these regulators ensure synchronized nuclear and plastid gene expression during chloroplast maturation.

Chloroplast biogenesis depends on the coordination between nuclear and plastid genomes. Most chloroplast proteins are nuclear-encoded and imported through the TRANSLOCON ON THE OUTER/INNER CHLOROPLAST ENVELOPE (TOC/TIC) complexes (Kessler and Schnell, 2009). Retrograde signals from developing plastids then communicate plastid status to the nucleus, mediated by the GUN1 protein, which ensures nuclear photosynthetic gene expression aligns with plastid functionality (Woodson et al., 2013; Martin et al., 2016). This two-way communication maintains stoichiometric balance between nuclear and plastid gene products, ensuring functional chloroplast assembly.

In parallel, phytohormones fine-tune greening progression. Auxin and other hormones such as cytokinin, ABA, GA and ethylene regulate the expression of certain nuclear and plastid genes through their signaling pathways. Auxin signaling is mediated by IAA and ARF proteins, which regulate important transcription factors like GLKs and HY5 during chloroplast development (Kobayashi et al., 2012, 2017; Yuan et al., 2018; Lupi et al., 2019). Cytokinin is a major positive regulator that promotes etioplast-to-chloroplast transition, chlorophyll biosynthesis, and cotyledon expansion (Cortleven et al., 2016). Cytokinin signaling through ARABIDOPSIS HISTIDINE KINASE (AHK)2/3 and ARABIDOPSIS RESPONSE REGULATOR (ARR)1/10/12 transcription factors upregulate HY5, GLK2, GNC, and CGA1, reinforcing photosynthetic gene expression including LHCB6 and HEMA1 (Argyros et al., 2008). It also enhances 5-AMINOLEVULINIC ACID (ALA) synthesis and stabilizes POR enzymes to accelerate chlorophyll production (Kusnetsov et al., 1998). GA promote greening by suppressing PIF activity through DELLA proteins and activating chlorophyll biosynthetic genes such as CHLH, PORC, and CAO (Cheminant et al., 2011). Ethylene exerts a dual role suppressing Pchlide accumulation in darkness while protecting cotyledons from photooxidative damage upon illumination through EIN3/EIL1-mediated activation of PORA/B (Zhong et al., 2009, 2010, 2014). BRs act synergistically with light via GATA2 to promote de-etiolation and chlorophyll synthesis (Sun et al., 2010), whereas ABA antagonizes greening until its suppression by CK through ARR-ABI5 interactions (Guan et al., 2014). Figure 2 illustrates the current understanding of how light and hormonal signaling pathways converge to coordinate chlorophyll biosynthesis, chloroplast differentiation, and the establishment of photosynthetic capacity during photomorphogenesis.

Ultimately, greening integrates light perception, transcriptional control, and hormonal regulation to establish photosynthetic competence. Light-mediated degradation of PIFs and stabilization of HY5 initiate chlorophyll biosynthesis, while cytokinin and GA amplify gene activation, and GUN1-mediated signaling synchronizes nuclear and plastid responses. These interdependent events transform the etioplasts of dark-grown seedlings into fully functional chloroplasts with developed thylakoid membranes, organized photosystems, and active electron transport chains. The process of greening thus exemplifies a precisely coordinated molecular program that enables a seedling to shift from a heterotrophic state dependent on stored reserves to a self-sustaining, photoautotrophic organism (Pogson and Albrecht, 2011; Zhelyazkova et al., 2012). Figure 4 presents the major light and hormone regulated factors implicated in greening and chloroplast development in a germinating seedling.

Development of root system architecture

Roots are the below ground organs of the plant and grow along the gravity, extending toward nutrient-rich zones in the soil to supply the plant with essential resources for optimal growth, survival, and productivity (Lacek et al., 2021). Although roots typically grow underground, they do not grow in complete darkness. Light is still able to penetrate several centimeters below the soil surface which significantly influences root growth, development, and architecture (Woolley and Stoller, 1978; Mo et al., 2015). Several reports have suggested that light can directly or indirectly modulate various aspects of root development including primary root elongation, lateral root initiation, root hair differentiation, and root gravitropic and phototropic responses (Burbach et al., 2012; Hopkins and Kiss, 2012; Wan et al., 2012; Mo et al., 2015). Roots can perceive light and evaluate its spectrum and intensity through multiple photoreceptors which enables them to coordinate the growth and development of organs above and below the ground (Mo et al., 2015). Figure 5 summarizes how light perceived in the shoot shapes root architecture by integrating photoreceptor signaling with sugar and hormone transport.

Phytochromes play a key role in regulating various physiological processes in the roots of Arabidopsis seedlings, such as promoting root elongation, initiating lateral root development, and mediating phototropic and gravitropic responses (Takano et al., 2001; Kiss et al., 2003; Costigan et al., 2011; Raya-González et al., 2014; Mo et al., 2015). PHYA, PHYB, PHYD, and PHYE are known to be expressed in the roots, whereas PHYC shows little to no detectable expression in root tissues (Van Gelderen et al., 2018a). Studies have shown that phyB and phyA single mutants as well as phyA phyB double mutants exhibit reduced root elongation compared to the wild type (Correll and Kiss, 2005; Silva-Navas et al., 2015). The initial report on R/FR light-mediated lateral root development was documented in pea wherein exposure to low-intensity red light suppressed lateral root initiation, while subsequent FR light treatment reversed this inhibition. These findings provided the first evidence implicating phytochromes in the regulation of lateral root formation (Furuya and Torrey, 1964). Furthermore, under low R/FR light conditions, various phytochromes control lateral root emergence via regulating the shoot to root auxin transport. Additionally, the transcript levels of auxin responsive genes including IAA1 and SHORT HYPOCOTYL 2 (SHY2) were reduced in the roots of phyA phyB double mutant (Reed et al., 1993; Salisbury et al., 2007). Recent research has revealed that low R/FR light perception by the shoot reduces the lateral root density by inhibiting LR emergence through phytochrome-dependent accumulation of HY5 in lateral root primordia, which decreases plasma membrane levels of the auxin transporters PIN3 and LAX3 (Van Gelderen et al., 2018a). Light-induced LONG HYPOCOTYL1 (HY1) plays a crucial role in phytochrome chromophore biosynthesis (Mahawar and Shekhawat, 2018). Transient expression of HY1 in the oscillation zone regulates pre-branch site formation, root meristem activity, and primary root elongation by modulating the oscillation signal. HY1 induces the expression of HY5 and HY5-HOMOLOG (HYH), which modulate auxin homeostasis in the oscillation zone through polar auxin transport. This regulation activates the oscillation signal, leading to periodic lateral root branching (Duan et al., 2021). Subsequently, another study revealed that direct illumination of roots with FR or R-light leads to primary root growth inhibition by affecting the auxin biosynthesis (Spaninks and Offringa, 2023). Under FR light, root-localized PHYA converts from its inactive (Pr) to active (Pfr) form and moves to the nucleus, where it suppresses PIF1 activity and reduces YUCCA4 (YUC4) and YUC6 expression. Similarly, under red light, PHYB switches from inactive (Pr) to active (Pfr) form and inhibits PIF4 and lowers YUC6 expression. Consequently, reduced YUC expression decreases auxin levels in the root apical meristem limiting root growth in FR and R-light conditions (Spaninks and Offringa, 2023). Recently, a study established the interconnection between GAs and HY5 in mediating lateral root growth under shade conditions (Van Gelderen et al., 2025). Supplemental FR light along with white light results in the shoot to root transport of GAs which causes DELLA degradation and indirectly enhances HY5 stability through an unknown mechanism (Van Gelderen et al., 2025). Growing evidence indicates that HY5 produced in the shoot is translocated to the roots in both Arabidopsis and tomato (Solanum lycopersicum), wherein HY5 functions locally to enhance root gravitropic responses, stimulate strigolactone biosynthesis, and activate the expression of light-responsive genes (Chen et al., 2016; Lee et al., 2016; Guo et al., 2021; Ge et al., 2022). Illumination of shoot activates the movement of HY5 to roots where it promotes the expression of NITRATE TRANSPORTER 2.1 (NRT2.1) thus, enhancing the nitrate uptake (Chen et al., 2016). Alternatively, it has been proposed that instead of auxin or HY5, photosynthetic sucrose acts as a long-distance shoot-to-root mobile signal and regulates the tryptophan-dependent auxin biosynthesis in the primary root tip, thus driving the lateral root clock to modulate the pace of lateral root initiation (Kircher and Schopfer, 2023). It has been established that hy5 mutant has greater number of lateral roots (Oyama et al., 1997). However, an additional mutation in CALMODULIN7 (CAM7) in the hy5 mutant leads to a significant decrease in the lateral root number (Abbas and Chattopadhyay, 2014). HY5 coordinates with auxin signaling to regulate key root hair development genes such as ROOT HAIR DEFECTIVE 6-LIKE 2 (RSL2), ROOT HAIR DEFECTIVE 6-LIKE 4 (RSL4), and EXPA7, which in turn control root hair growth through cell wall-related pathways. It also influences cell wall genes like REDUCED RESIDUAL ARABINOSE1 (RRA1) and REDUCED RESIDUAL ARABINOSE2 (RRA2) via miR397b, although the mechanism behind HY5’s direct regulation of these cell wall genes is still uncertain (Gaddam et al., 2024; Ku, 2024).

Both CRY1 and CRY2 transcripts as well as proteins are expressed in roots. However, CRY2 protein was detected in dark treated roots (Canamero et al., 2006). Mutants of CRY1 exhibit reduced primary root growth whereas the overexpression lines display enhanced root growth. Thus, CRY1 positively regulates root elongation in blue light. In contrast, cry2 mutant shows an opposite root elongation phenotype compared to cry1 mutant, indicating antagonistic functions of these two photoreceptors (Canamero et al., 2006). Because cryptochrome signaling is perceived in the shoot and 1-N-naphthylphthalamic acid (NPA) abolishes their differential effects, blue-light regulation of root growth appears to be mediated by shoot-derived auxin-dependent signaling (Canamero et al., 2006; Mo et al., 2015). In addition, CRY1 acts as a negative regulator of lateral root development as CRY1-overexpressing seedlings displayed significantly reduced lateral root growth in blue light (Zeng et al., 2010). Moreover, the CRY1 overexpression had reduced PIN1 expression and diminished free IAA levels indicating that CRY1 constrains lateral root formation largely through its inhibitory influence on auxin transport (Zeng et al., 2010). Recently, it has been revealed that CRY2 functions in darkness to modulate root development by repressing FORKED LIKE 1 (FL1) and FORKED LIKE 3 (FL3). FL1 and FL3 associate with the chromatin of cell-division genes to promote their transcription. However, CRY2 physically interacts with FL1 and FL3 and inhibits their activity to suppress root elongation in dark (Zeng et al., 2025).

Another set of blue light photoreceptors are phototropins which are plasma membrane localized receptors and promote plant growth by regulating a light capturing phenomenon known as phototropism (Yun et al., 2023b; Rawat and Laxmi, 2024). Along with shoot, PHOT1 is also expressed in roots and regulates various root developmental responses (Van Gelderen et al., 2018b). PHOT1 mediates an important role in blue light induced negative phototropism of roots. Blue light-induced negative root phototropism operates through the PHOT1/NON-PHOTOTROPIC HYPOCOTYL 3 (NPH3) signaling module, which enhances shootward auxin transport in the root apex. This response is mediated by PHOT1/NPH3-dependent reallocation of PIN2 from intracellular compartments to the plasma membrane (Wan et al., 2012). Furthermore, PHOT1 also governs the regulation of primary root growth. Interestingly, PHOT1 increases the drought resistance and allows enhanced growth efficiency of plant roots in dry soils to ensure adequate water absorption (Galen et al., 2007). It has been established that PHOT1 also controls lateral root growth in Arabidopsis (Moni et al., 2015). PHOT1 is strongly expressed in the lateral root elongation zone, coinciding with sites of high auxin accumulation. Consistent with this, phot1 mutants exhibit increased lateral root epidermal growth, number, and density under both blue and white light, supporting a regulatory role for PHOT1 in lateral root development (Moni et al., 2015).

Plants also perceive low fluence rates of UV-B as a regulatory signal to control photomorphogenesis (Yokawa et al., 2016; Lee et al., 2017). UVR8 functions as the primary UV-B photoreceptor and plays a central role in mediating UV-B–induced photomorphogenesis and acclimation responses in plants (Liang et al., 2019). Recent work has shown that Arabidopsis roots display negative phototropism under low fluence UV-B. Unilateral UV-B exposure causes auxin to accumulate on the shaded side, thus inhibiting cell elongation and driving the root to bend away from the UV-B source (Yokawa et al., 2016). Fasano et al., 2014 reported the role of UVR8 in modulating the root system architecture. The UVR8 overexpression plants exhibited perturbed primary and lateral root development as a result of flavonoid accumulation which contributed to the changes in the auxin transport (Fasano et al., 2014). Apart from UVR8, it has also been identified that ROOT UV-B SENSITIVE 1 (RUS1) and RUS2 which are root specific proteins, participate in UV-B perception and signaling (Leasure et al., 2009; Lee et al., 2017). Consequently, rus1 and rus2 mutants exhibit defective root growth and development under UV-B conditions. Nonetheless, the specific photoreceptor(s) underlying RUS-dependent regulation of root growth has yet to be identified (Leasure et al., 2009; Lee et al., 2017).

Ultimately, the plasticity of the root system is achieved through a sophisticated integration of localized light perception and long-distance signals from the shoot, ensuring that root architecture is continuously optimized in response to the surrounding light environment.

Conclusion and future perspectives

Early seedling development represents a sophisticated example of how plants interpret environmental cues to guide critical developmental decisions. Light acts as the primary regulatory signal driving the transition from skotomorphogenesis to photomorphogenesis, orchestrating the shift from heterotrophic growth to photoautotrophic establishment. This transition, beginning at germination and extending through the formation of shoot and root systems, is governed by a tightly interconnected network of photoreceptors, transcription factors, phytohormones, and epigenetic regulators. Rather than functioning as independent pathways, these components operate as an integrated signaling framework that coordinates development across tissues and enables seedlings to adjust growth in response to continuously changing environmental conditions.

Over the past decades, research has revealed that photomorphogenesis is far more complex than a simple light-triggered developmental switch. It is intricately interwoven with major hormonal, transcriptional, and metabolic networks, creating a multilayered regulatory system that provides remarkable developmental plasticity (Huq et al., 2024). These components function in a highly coordinated manner across tissues to ensure synchronized development. From the decision to germinate to the establishment of root architecture, light acts as a master signal that enables seedlings to adjust their developmental programs in response to changing environmental conditions. At the same time, the ongoing discovery of new signaling components and regulatory interactions continues to expand this framework, highlighting that our current understanding remains incomplete and that many key mechanistic questions are still unresolved (Pradhan et al., 2026).

A significant limitation of current research is the tendency to study aspects of seedling development in isolation. While this has yielded valuable mechanistic insights, it fails to capture the holistic synergy of multiple signaling pathways. The molecular mediators facilitating crosstalk among the diverse processes governing seedling establishment remain only partially understood. Unraveling these interconnections will be essential to identifying the regulatory nodes that coordinate seedling development as a dynamic, integrated system.

One compelling outstanding question concerns the molecular function of HLS1, a central regulator integrating light and hormonal cues during apical hook development. Although its genetic importance is well-documented, the biochemical activity of HLS1 and the mechanisms through which it coordinates transcriptional and epigenetic regulation remains elusive (Mazzella et al., 2014). Resolving the HLS1 mechanism will provide vital insights into how signaling pathways converge to control developmental transitions (Li et al., 2004; Liao et al., 2016).

Furthermore, there is an increasing recognition that light influences plant development through mechanisms that may operate independently of canonical photoreceptor-mediated signaling cascades. This is particularly evident in the root system, which exhibits complex interactions with light despite its subterranean nature (Wan et al., 2019). Beyond classical signaling, light serves as a potent modulator of nutrient homeostasis and mineral translocation. For instance, light availability significantly influences the primary root growth response to phosphate starvation, where transcriptional landscapes differ vastly between light-exposed and dark-grown roots (Wang et al., 2025). Similarly, light-driven processes have been shown to regulate iron translocation in the xylem, mediated by ferroxidases such as LOW PHOSPHATE ROOT 1 (LPR1) and LPR2, which are essential for maintaining systemic nutrient balance (Xu et al., 2022).

These findings underscore the need for refined experimental methodologies. In nature, roots grow in darkness while shoots perceive light above the soil. Many standard laboratory systems expose the entire seedling to uniform illumination, which can trigger excessive reactive oxygen species (ROS) production (Yokawa et al., 2014) and alter cytokinin homeostasis (Novák et al., 2015). Such physiological artifacts can confound interpretations of how plants respond to nutrient availability, salinity, and hormonal signals (Mo et al., 2015; Silva‐Navas et al., 2015; Wan et al., 2019; Zheng et al., 2019; Miotto et al., 2021). Specialized platforms, such as the Dark-Root (D-Root) system, offer a more realistic framework for investigating shoot-root communication and root system architecture by maintaining roots in darkness (Miotto et al., 2019, 2021; Dermendjiev et al., 2023).

Looking forward, the integration of advanced technologies including single-cell transcriptomics, chromatin profiling, live imaging, and computational modeling will be essential for uncovering how light-regulated networks operate across specific cell types and tissues. Furthermore, extending these studies to crop species under environmentally relevant conditions will bridge the gap between fundamental molecular discoveries and practical agricultural applications.

In summary, seed germination and early seedling development are highly coordinated, adaptive processes with light serving as the master environmental signal. By acting through interconnected hormonal and epigenetic networks, and through emerging non-canonical pathways, light allows seedlings to fine-tune their programs for optimal survival. Bridging the remaining gaps between molecular mechanisms and whole-plant responses will not only deepen our understanding of plant plasticity but also provide new strategies to enhance crop establishment and resilience in a changing climate.

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Footnotes

Edited by: Jay Prakash Maurya, Banaras Hindu University, India

Reviewed by: Gouranga Upadhyaya, Jadavpur University, India

Zheng Zai, Chinese Academy of Tropical Agricultural Sciences, China

Mouna Ghorbel, University of Hail, Saudi Arabia