The switch from dark- to light-mediated development is critical for the survival and growth of seedlings, but the underlying regulatory mechanisms are incomplete. Here, we show that the steroids phytohormone brassinosteroids play crucial roles during this developmental transition by regulating chlorophyll biosynthesis to promote greening of etiolated seedlings upon light exposure. Etiolated seedlings of the brassinosteroids-deficient det2-1 (de-etiolated2) mutant accumulated excess protochlorophyllide, resulting in photo-oxidative damage upon exposure to light. Conversely, the gain-of-function mutant bzr1-1D (brassinazole-resistant 1-1D) suppressed the protochlorophyllide accumulation of det2-1, thereby promoting greening of etiolated seedlings. Genetic analysis indicated that phytochrome-interacting factors (PIFs) were required for BZR1-mediated seedling greening. Furthermore, we reveal that GROWTH REGULATING FACTOR 7 (GRF7) and GRF8 are induced by BZR1 and PIF4 to repress chlorophyll biosynthesis and promote seedling greening. Suppression of GRFs function by overexpressing microRNA396a caused an accumulation of protochlorophyllide in the dark and severe photobleaching upon light exposure. Additionally, BZR1, PIF4, and GRF7 interact with each other and precisely regulate the expression of chlorophyll biosynthetic genes. Our findings reveal an essential role for BRs in promoting seedling development and survival during the initial emergence of seedlings from subterranean darkness into sunlight.

从暗介导的发育到光介导的发育的转变对于幼苗的生存和生长至关重要，但潜在的调节机制并不完整。在这里，我们表明类固醇植物激素油菜素类固醇通过调节叶绿素生物合成以促进黄化幼苗在光照下变绿，在这一发育转变过程中发挥着至关重要的作用。油菜素类固醇缺陷的det2-1 ( de-etiolated2 ) 突变体的黄化幼苗积累了过量的原叶绿素，导致暴露在光下时发生光氧化损伤。相反，功能获得突变体bzr1-1D （抗油菜素唑1-1D ）抑制det2-1原叶绿素的积累，从而促进黄化幼苗的绿化。遗传分析表明，BZR1 介导的幼苗绿化需要光敏色素相互作用因子 (PIF)。此外，我们还发现，BZR1 和 PIF4 诱导生长调节因子 7 ( GRF7 ) 和GRF8抑制叶绿素生物合成并促进幼苗绿化。通过过度表达microRNA396a来抑制 GRF 功能会导致原叶绿素在黑暗中积累，并在光照下导致严重的光漂白。此外，BZR1、PIF4和GRF7相互作用并精确调节叶绿素生物合成基因的表达。我们的研究结果揭示了在幼苗从地下黑暗进入阳光的最初出苗过程中，BR 在促进幼苗发育和存活方面发挥着重要作用。