Alem Antonela L, Gonzalez Daniel H, Viola Ivana L
Instituto de Agrobiotecnología del Litoral (CONICET-UNL), Cátedra de Biología Celular y Molecular, Facultad de Bioquímica y Ciencias Biológicas, Universidad Nacional del Litoral, 3000, Santa Fe, Argentina.
New Phytol. 2025 Oct;248(1):265-281. doi: 10.1111/nph.70407. Epub 2025 Jul 24.
Cotyledon de-etiolation is a crucial process during seedling photomorphogenesis that comprises growth pattern reprogramming and the development of photosynthetically active chloroplasts. Studying this process at the molecular level is essential to understand how plants successfully transition to autotrophic metabolism. We studied the role of the Arabidopsis class II TEOSINTE BRANCHED1, CYCLOIDEA, and PCF (TCP) transcription factor TCP10 in cotyledon de-etiolation using a variety of phenotypic, genetic, and molecular approaches. We found that TCP10 is a positive regulator of cotyledon photomorphogenesis that promotes expression of photosynthesis and cotyledon opening genes during de-etiolation, acting either directly or through the central regulator of photomorphogenic development GOLDEN2-LIKE1 (GLK1). Furthermore, TCP10 and GLK1 form a direct positive transcriptional loop that coordinates gene expression responses during de-etiolation. Besides, while light induces TCP10 expression in cotyledons of dark-germinated seedlings to trigger photomorphogenesis, retrograde signals emitted from damaged plastids prevent its expression and induce TCP10 protein degradation via the 26S proteasome, thereby preventing TCP10-induced target gene expression and cotyledon de-etiolation under these conditions. We propose that the TCP10-GLK1 transcriptional module acts as a hub that integrates light and plastid retrograde signaling pathways to fine-tune de-etiolation and ensure successful early seedling establishment according to internal and environmental stimuli.
子叶脱黄化是幼苗光形态建成过程中的一个关键过程，包括生长模式重编程和光合活性叶绿体的发育。在分子水平上研究这一过程对于理解植物如何成功过渡到自养代谢至关重要。我们使用多种表型、遗传和分子方法研究了拟南芥II类TEOSINTE BRANCHED1、CYCLOIDEA和PCF（TCP）转录因子TCP10在子叶脱黄化中的作用。我们发现TCP10是子叶光形态建成的正调控因子，在脱黄化过程中促进光合作用和子叶开放基因的表达，其作用方式是直接作用或通过光形态建成发育的中心调控因子类黄金2（GLK1）发挥作用。此外，TCP10和GLK1形成一个直接的正转录环，在脱黄化过程中协调基因表达反应。此外，虽然光诱导暗发芽幼苗子叶中TCP10的表达以触发光形态建成，但受损质体发出的逆行信号会阻止其表达，并通过26S蛋白酶体诱导TCP10蛋白降解，从而在这些条件下阻止TCP10诱导的靶基因表达和子叶脱黄化。我们提出，TCP10 - GLK1转录模块作为一个枢纽，整合光和质体逆行信号通路，以微调脱黄化过程，并根据内部和环境刺激确保幼苗早期成功建立。
