TSC1 enables plastid development under dark conditions, contributing to rice adaptation to transplantation shock

Since its domestication from wild rice thousands of years ago, rice has been cultivated largely through transplantation. During transplantation from the nursery to the paddy field, rice seedlings experience transplantation shock which affects their physiology and production.However, the mechanisms underlying transplantation shock and rice adaptation to this shock are largely unknown. Here,we isolated a transplant-sensitive chloroplast-deficient（tsc_1）rice mutant that produces albino leaves after transplantation.Blocking light from reaching the juvenile leaves and leaf primordia caused chloroplast deficiencies in transplanted tsc_1 seedlings. TSC_1 encodes a noncanonical adenosine triphosphate-binding cassette（ABC） transporter homologous to At NAP_（14） and is of cyanobacterial origin. We demonstrate that TSC_1 controls plastid development in rice under dark conditions, and functions independently of light signaling.However, light rescued the tsc_1 mutant phenotype in a spectrum-independent manner. TSC_1 was upregulated following transplantation, and modulated the iron and copper levels, thereby regulating prolamellar body formation during the early P_4 stage of leaf development. Therefore, TSC_1 is indispensable for plastid development in the absence of light,and contributes to adaptation to transplantation shock.Our study provides insight into the regulation of plastid development and establishes a framework for improving recovery from transplantation shock in rice.

Ultrastructural studies of seed coat and cotyledon during rapeseed maturation

Brassica napus L.(B.napus)is an important oil crop worldwide and it rapidly accumulates oil at late stage of seed maturation.However,little is known about the cellular mechanism of oil accumulation and seed color changes during the late stage of rapeseed development.Here,we analyzed the ultrastructure of seed coat,aleurone and cotyledon in embryos of B.napus from 25 to 70 days after flowering(DAF).The pigments,which were deposited on the cell wall of palisade cells in seed coat,determined dark black color of rapeseed.The chloroplasts degenerated into non-photosynthetic plastids which caused the green cotyledon to turn into yellow.The chloroplasts in aleurone and cotyledon cells respectively degenerated into remnants without inner and outer envelope membranes and ecoplasts with intact inner and outer envelope membranes.From 40 to 70 DAF,there were degraded chloroplasts without thylakoid,oil bodies contacting with plastids or protein bodies,big starch deposits of chloroplasts degrading into small particles then disappearing,and small endoplasmic reticulum(ER)in aleurone and cotyledon cells.Additionally,there were decreases of chlorophyll content and dramatic increases of oil content in rapeseed.These results suggested that the rapid oil accumulation was independent on the NADPH synthesized by photosynthesis of chloroplasts and probably utilized other sources of reductant,such as the oxidative pentose phosphate pathway during the late stage of rapeseed development.The triacylglycerol assembly presumably utilizes the enzymes in the plastid,cytosol or oil body of cotyledon and aleurone cells.

植物叶绿体发育及调控研究进展

植物的光合作用几乎是所有生物生存和发展的物质基础。叶绿体是绿色植物进行光合作用的重要细胞器。尽管叶绿体发育及调控一直受到人们的关注,但其装备及调控的分子机制尚不完全清楚。该文对叶绿体装备过程、叶绿体发育调控及质体-细胞核反向信号的研究进展进行概述,以使人们从整体上认识叶绿体发育及调控机制。

Phosphorylation of WHIRLY1 by CIPK14 Shifts Its Localization and Dual Functions in Arabidopsis

Plastid-to-nucleus retrograde signaling is critical for normal growth and development in plants. The dualfunction and dual-located ssDNA binding protein WHIRLY1 （WHY1） has been proposed to coordinate the retrograde signaling from plastids to the nucleus. However, the regulatory mechanism governing the functional switch of WHY1 for mediating plastid-to-nucleus retrograde signaling remains unknown. Here, we report that the Calcineurin B-Like-Interacting Protein Kinase14 （CIPK14） interacts with and phosphorylates WHY1 in Arabidopsis. Phosphorylation of WHY1 results in increased accumulation in the nucleus and enhanced binding with the promoter of WRKY53, which encodes a key transcription factor regulating leaf senescence in Arabidopsis. Transgenic plants overexpressing CIPK14 showed an increased nuclear isoform but decreased plastid isoform of WHY1, among which 95% of transgenic lines showed the stay-green phenotype and 5% of lines showed the variegated pale-green phenotype. Interestingly, the phenotypes of both types of transgenic plants could be recovered by overexpression of plastid-form WHY1. In contrast, knockdown of ClPK14 caused early senescence and even seedling-lethal phenotypes along with elevated expression of senescence-related genes such as WRKY53, SAG12, and NDHF but decreased expression of MER11, RAD50, and POR genes, which could be rescued by overexpression of CIPK14 but not by overexpressing plastid-form or nuclear-form WHY1; the stay-green plants overexpressing ClPK14 showed reduced expression of WRKY53, SAG12, NDHF, and large plastid rRNA. Consistently, the accu- mulation of nuclear-form WHY1 was significantly reduced in the CIPK14 knockdown lines, resulting in a low ratio of nuclear-/plastid-form WHY1. Taken together, our results demonstrate that CIPK14 regu- lates the phosphorylation and organeUar distributions of WHY1 and pinpoint that ClPK14 may function as a cellular switch between leaf senescence and plastid development for coordinating the intercellular signaling in Arabidopsis.