Role of Phytohormones and Light in De-etiolation
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Role of Phytohormones and Light in De-etiolation V. V. Kusnetsova, *, A. S. Doroshenkoa, N. V. Kudryakovaa, and M. N. Danilovaa aTimiryazev
Institute of Plant Physiology, Russian Academy of Sciences, Moscow, 127276 Russia *e-mail: [email protected] Received April 24, 2020; revised April 27, 2020; accepted April 27, 2020
Abstract—De-etiolation or transition from etiolated growth (skotomorphogenesis) to photomorphogenesis is one of the most intriguing and intricate stages of plant ontogenesis. It comprises reprogramming of plant cell metabolism, reorganizing the operation of the hormonal system, and altering plant morphology. Dark growth in the soil mainly depends on phytohormones with gibberellins and brassinosteroids playing the leading role; on the soil surface, light as a major exogenous agent starts operating. It inhibits activity of the main repressor of photomorphogenesis (COP1) and regulators of transcription, which govern realization of gibberellin (DELLA) and brassinosteroid (BZR1/BES1) signals and activates trans-factors initiating transition to autotrophic nutrition (for instance, HY5). The strategy of etiolated growth consists in achieving a quick exposure to sunlight at the expense of active elongation of the stem. For transition to autotrophic nutrition, a plant must form a photosynthetic apparatus and protect itself from possible light injury. This review deals with the role of the main regulatory components ensuring etiolated growth and transition to photomorphogenic development. Keywords: photoreceptors, trans-factors, phytohormones, photomorphogenesis, etiolation DOI: 10.1134/S1021443720060102
INTRODUCTION Depending on the absence or availability of light, young seedlings pursue one of the two programs of development: etiolated growth (skotomorphogenesis) or de-etiolation (photomorphogenesis), respectively [1–3]. Etiolated dicotyledons produce an apical hook for protection of the apical meristem; they lack leaves and have proplastids and etioplasts instead of chloroplasts. In the case of etiolation, the bulk of storage substances of the seed are spent on the quick growth of the hypocotyl. Prolonged stay in the dark may result in depletion of nutrients and irreversible etiolation, which may cause a loss of seedlings. Etiolation is achieved by inhibition of expression of the genes responsible for Abbreviations: BES1—BRI1-EMS-suppressor 1 or BZR2; bHLH—basic helix-loop-helix; BIN2—brassinosteroid insensitive 2; BR—brassinosteroids; BZR1—brassinazole-resistant 1; Chlide—chlorophyllide; ChlH—Mg-chelatase H subunit; CK— cytokinins; СОР1—constitutive photomorphogenesis 1; СRY— cryptochrome; DELLA domain—Asp-Glu-Leu-Leu-Ala motif; FHL—FHY1-like protein; FHY—far-red elongated hypocotyl 1; EIL1—ethylene insensitive 3-like 1; EIN3—ethylene insensitive 3; GA—gibberellins; GID1—gibberellin insensitive dwarf 1; GNC (GATA, nitrate inducible, carbon-metabolism involved) and GNL/CGA1 (GNC-like/cytokinin-responsive gata factor 1)— trans-factors of GATA type; HFR1—long hypocotyl in far-red 1; HY5—elongated
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