A recent review published in Frontiers in Plant Physiology by researchers at the Indian Institute of Science Education and Research in Bhopal takes a broader view of this process, tracing light signaling pathways across the green lineage from unicellular algae to mosses, liverworts, and flowering plants. The evolutionary-developmental, or evo-devo, perspective is essential because the light environment changed dramatically when plants left water for land. Light quality and quantity differ enormously between aquatic and terrestrial habitats, and understanding how early land plants adapted their light-sensing systems to this shift offers clues about how the entire photosynthetic toolkit was assembled over hundreds of millions of years.

In Arabidopsis, light perception begins with a small set of photoreceptors, each tuned to a specific part of the spectrum. Cryptochromes, phototropins, ZEITLUPE, FKF1, and LKP2 detect blue light, while the phytochromes sense red and far-red wavelengths. The UV RESISTANCE LOCUS 8 (UVR8) photoreceptor handles ultraviolet-B. Phytochromes exist in two photoconvertible states: the Pr form absorbs red light and converts to the active Pfr form, which moves into the nucleus to regulate downstream signaling; far-red light reverses the process. Arabidopsis carries five phytochromes, with Phytochrome A specialized for far-red responses and Phytochrome B serving as the primary red-light receptor. Once activated, these photoreceptors converge on a shared set of transcriptional regulators, most notably ELONGATED HYPOCOTYL 5 (HY5) and the B-BOX (BBX) family of proteins, which orchestrate the gene expression changes that drive photomorphogenesis.

The mechanics of hypocotyl elongation illustrate how tightly light and hormone signaling are interwoven. In darkness, PHYTOCHROME INTERACTING FACTORS (PIFs) accumulate and promote gibberellic acid biosynthesis, which in turn activates auxin production. PIFs also physically interact with DELLA proteins to promote their degradation, removing a brake on growth. The resulting auxin surge triggers SMALL AUXIN UP-RNA (SAUR) genes, which inhibit PP2C.D phosphatases and activate proton pumps that acidify the cell wall, allowing EXPANSIN and XTH enzymes to loosen the wall matrix so cells can expand. In parallel, the E3 ubiquitin ligase COP1, nuclear-localized in the dark, degrades the phosphorylated form of BES1 and stabilizes the brassinosteroid-responsive transcription factors BZR1 and BES1, which cooperate with PIFs to sustain elongation. DET1 adds another layer by increasing PIF abundance through negative regulation of DELLA proteins.

When light arrives, this entire growth-promoting network is dismantled through multiple parallel mechanisms. Phototropin 1 rapidly inhibits proton pump activation below the hypocotyl apex, while cryptochrome 1 stabilizes AUX/IAA repressors to suppress auxin signaling in the apical zone. CRY1 also physically interacts with the gibberellin receptor GID1, weakening the GID1-DELLA interaction and allowing DELLA proteins to accumulate and inhibit PIFs. In red light, activated phyB triggers PIF degradation and stabilizes HEMERA to promote the breakdown of PIF1 and PIF3 in nuclear photobodies. HY5 competes with PIFs for binding to promoters of auxin biosynthesis genes such as YUC8, recruits histone deacetylase HDA15 to silence cell wall and auxin genes through chromatin modification, and works alongside BBX proteins like BBX9, BBX14, BBX15, and BBX16, which form feedback loops with both HY5 and PIFs to fine-tune the balance between growth and photomorphogenic arrest.

Cotyledon opening and greening represent the second half of de-etiolation, and they depend on a distinct set of molecular players. In the dark, COP1 and PIFs hold cotyledons closed; mutants lacking these factors open their cotyledons even without light. The SAUR gene family provides a striking example of antagonistic regulation: SAUR17, highly expressed in etiolated cotyledons and the apical hook, maintains the closed state by sequestering PP2C-D1 away from SAUR50, while the light-induced lirSAUR subgroup, including SAUR16 and SAUR50, promotes opening by inhibiting the same phosphatase. TCP transcription factors add another layer of control. CIN-like TCP genes such as TCP3, TCP4, and TCP10 promote cotyledon opening by directly activating SAUR16 and SAUR50, but dark-accumulated PIF3 antagonizes TCP4 binding to SAUR promoters. TCP15 requires the chloroplast regulator GLK1 to induce both cell expansion genes and photosynthesis-associated nuclear genes, linking morphological opening to the establishment of the photosynthetic apparatus.

Brassinosteroid and jasmonate hormones modulate this transition in opposing ways. BZR1 induces auxin-related genes including LAX3, WAG2, PIN1, and ACS5 to suppress cotyledon opening, while HY5 inhibits BZR1 activity and prevents its binding to those promoters. The BBX family again serves as an integration hub: BBX32, induced by brassinosteroid in cotyledons, physically interacts with both BZR1 and PIF3 to suppress opening in darkness, whereas BZS1 (BBX20) enhances light signaling while repressing brassinosteroid responses and undergoes COP1-mediated degradation. BBX28 and BBX29 positively regulate brassinosteroid signaling in a BRI1- and BIN2-dependent manner. Jasmonate, meanwhile, promotes cotyledon opening by inhibiting COP1 and stabilizing HY5 and the PAR1/PAR2 proteins, revealing that a defense hormone participates directly in the photomorphogenic switch.

Greening itself carries lethal risks if mismanaged. Chlorophyll biosynthesis proceeds from glutamate through 5-aminolevulinic acid and the tetrapyrrole pathway to protoporphyrin IX, which Mg-chelatase converts toward protochlorophyllide. In dark-grown seedlings, plastids exist as etioplasts that accumulate protochlorophyllide, and upon light exposure, protochlorophyllide oxidoreductase enzymes catalyze the conversion to active chlorophyll. Excess protochlorophyllide generates reactive oxygen species upon illumination, causing photooxidative damage or cell death. The FLU protein provides post-translational feedback control by complexing with CHL27, PORB, and PORC to inhibit glutamyl-tRNA reductase and curb 5-aminolevulinic acid synthesis. Transcriptionally, PIFs repress tetrapyrrole biosynthetic genes including CAO, HEMA1, GUN4, and GUN5 while simultaneously activating ROS-scavenging genes like APX2 and ZAT10, a dual strategy that limits pigment accumulation and prepares antioxidant defenses. Recent work has identified BBX10 and BBX11 as additional safeguards, with BBX10 interacting with PIF1 to prevent photooxidation and BBX11 acting downstream of PIF3 in the dark before HY5 activates it in light.

The evolutionary dimension of this review emerges most clearly in the comparison with Chlamydomonas reinhardtii, a unicellular green alga whose light-sensing apparatus differs fundamentally from that of land plants. Chlamydomonas perceives light through a specialized eyespot organelle and an array of photoreceptors including channelrhodopsins, cryptochromes, UVR8, and phototropins. Channelrhodopsins CHR1 and CHR2 function as light-gated cation channels that trigger membrane depolarization and alter flagellar beating, enabling positive or negative phototaxis. Notably, phytochromes have not been reported in Chlamydomonas, marking a major divergence from land plants. The alga does, however, possess a UV-B sensing protein, Cr-UVR8, whose tryptophan residues and monomerization upon UV-B exposure closely parallel the angiosperm mechanism, and Cr-UVR8 can functionally complement Arabidopsis uvr8 null mutants. Cryptochromes in Chlamydomonas span plant-like, animal-like, and DASH subfamilies, with the animal-like aCRY responding to both blue and red wavelengths and regulating zygote germination, mating, and DNA repair. The single phototropin CrPhot controls sexual reproduction, starch metabolism through the PMSK1-GAP1 pathway, eyespot size, and channelrhodopsin levels, demonstrating that a single blue-light receptor can coordinate development, metabolism, and behavior in a unicellular organism.

In the bryophytes, the picture becomes more recognizably plant-like but reveals instructive simplifications. Marchantia polymorpha carries single copies of most light signaling factors, including one phytochrome, one cryptochrome, one UVR8, and one PIF. The MpPHY-MpPIF module governs gemma germination, sexual reproduction, and meristem dormancy through a liverwort-specific microRNA, Mp-MR13, which represses the branching regulator MpSPL1. Under white light, reduced MpPIF allows Mp-MR13 to accumulate, breaking meristem dormancy and promoting dichotomous branching; in shade, elevated MpPIF suppresses the microRNA and maintains dormancy. Physcomitrium patens, by contrast, has expanded its light signaling repertoire, with seven phytochromes, nine COP1 orthologs, four phototropins, and two each of cryptochromes, HY5, and SPA proteins. Despite this expansion, the core logic remains conserved: PpPHY5abc mediates red-light responses, PpPHY1/3 handles far-red, PpCRYs regulate protonemal branching and gametophore development, and the PpCOP1-PpSPA complex represses light-responsive genes in darkness, though mutants lacking these factors still show partially constitutive light responses, suggesting additional repressors await discovery. Taken together, the review argues that the fundamental architecture of light perception and signal transduction is conserved across the green lineage, while gene copy number, photoreceptor composition, and downstream wiring have diverged substantially, offering a framework for understanding how plants conquered the terrestrial light environment and how future tools like single-cell transcriptomics and optogenetics might further illuminate this evolutionary story.

Subject of Research: Evolutionary conservation and divergence of light signaling pathways regulating early plant development across algae, bryophytes, and Arabidopsis

Article Title: Light signaling pathways regulating early plant development: an evo-devo approach

Article References: Pradhan, A. A., Rao, K. V., Suyal, S., Singh, N., Zadoo, U., & Datta, S. (2026). Light signaling pathways regulating early plant development: an evo-devo approach. Frontiers in Plant Physiology, 4, Article 1722598. https://doi.org/10.3389/fphgy.2026.1722598

Image Credits: AI Generated

DOI: 10.3389/fphgy.2026.1722598

Keywords: light signaling, photomorphogenesis, de-etiolation, phytochrome, cryptochrome, Chlamydomonas reinhardtii, Marchantia polymorpha, Physcomitrium patens, Arabidopsis thaliana, chloroplast biogenesis, HY5, PIF