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On April 10, the international academic journal Nature Plants published online the latest research paper by the Guo Fangqing Research Group of the Center for Excellence in Molecular Plant Sciences of the Chinese Academy of Sciences/Institute for Plant Physiology and Ecology, entitled SPL6 Represses Signals outputs of ER Stress in control of panicle cell in the rice.
results reveal editing of rice SBP-box family transcription factor SPL6 inhibits the transcription of intracellular intracellular stress sensing factor (ER-strelient sensor) IRE1, controls the output strength of the stress signal;
therefore, SPL6, as the upstream regulation key factor of the signal path of the endoblastnetwork, regulates the space-time intensity and balance of the stress signal output, and then determines the fate of cell survival in the development of rice spike.
the albino phenomenon caused by the degradation of the top of the rice spike (commonly known as "balding") is a disadvantage in the process of rice production practice, resulting in a significant reduction in the number of grain grains per spike, a significant decrease in the solidity rate, seriously affecting rice yield.
breeders found that the degradation of the small spike at the top of the rice spike was affected by cultivated environmental conditions such as temperature and humidity.
in the process of deciphering the genetic mechanism of the degradation of the small spike at the top of the rice, Guo Fangqing's research group adopted different strategies and technical paths from previous researchers.
, by using the means of reverse genetics, from the high-throughput screening and acquisition of rice spike development-specific expression transcription factor genes, screened a number of special expression in the development of rice spike as the focus of the study object.
found that the rice SBP-box family transcription factor SPL6 functional lysator showed a significant spike top degradation of the "vulture" phenotype.
genetic complementarity experiments show that the top spike degenerative phenotype of the mutant is caused by the SPL6 mutation.
cytology and biochemical analysis showed that the top spike of the spl6 mutant showed significant cellular procedural death (PCD) characteristics under normal growth conditions.
based on systematic analysis of the downstream regulatory target gene, it was found that the transcription level and protein level of IRE1 of the small spike cell endoblast icing network at the top of the SPL6 mutant were significantly increased.
multiple molecular biology and biochemical evidence, SPL6 inhibits the expression of IRE1 as a transcription factor through a specific binding IRE1 promoter.
through SPL6 promoter, tissue-specific interference (RNAi) SPL6 mutation in the body IRE1 expression level, can partially restore the top small spike degenerative phetype, for the high level of IRE1 expression caused by the mutant spike "bald" characteristics to establish a genetic link.
the internal network stress sensing factor IRE1 has both the activity of protein kinase and nucleic acid endoenzyme.
the uncontrolled accumulation of IRE1 protein in the mutant strain initiated a large number of shearing of downstream target gene bZIP50 transcription factor mRNA, after translation of the bZIP50 protein into the nucleus to activate the expression of its downstream regulatory gene, including a large number of PCD-related marker genes, resulting in cells under normal growth conditions in the internal mesh stressed excessive state, and eventually caused cell aging degradation and spike "baldness" characteristics.
laboratory staff Member Wang Qinglong as the first author of the paper to undertake most of the research work.
the work has been supported by the Chinese Academy of Sciences Pilot B Cultivation Project, the Ministry of Science and Technology and the National Natural Science Foundation of China.
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