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赤霉素受体GID1a、GID1b和GID1c在不依赖Sly1的赤霉素信号传导中的作用。

The roles of the GA receptors GID1a, GID1b, and GID1c in sly1-independent GA signaling.

作者信息

Hauvermale Amber L, Ariizumi Tohru, Steber Camille M

机构信息

Department of Crop and Soil Science; Washington State University; Pullman, WA USA.

Department of Crop and Soil Science; Washington State University; Pullman, WA USA; USDA-ARS; Wheat Genetics; Quality Physiology and Disease Research Unit; Pullman, WA USA.

出版信息

Plant Signal Behav. 2014;9(2):e28030. doi: 10.4161/psb.28030. Epub 2014 Feb 12.

DOI:10.4161/psb.28030
PMID:24521922
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4091331/
Abstract

Gibberellin (GA) hormone signaling occurs through proteolytic and non-proteolytic mechanisms. GA binding to the GA receptor GID1 (GA-INSENSITIVE DWARF1) enables GID1 to bind negative regulators of GA responses called DELLA proteins. In proteolytic GA signaling, the SLEEPY1 (SLY1) F-box protein targets DELLA proteins in the GID1-GA-DELLA complex for destruction through the ubiquitin-proteasome pathway. Non-proteolytic GA signaling in sly1 mutants where GA cannot target DELLA proteins for destruction, requires GA and GID1 gene function. Based on comparison of gid1 multiple mutants to sly1 gid1 mutants, GID1a is the primary GA receptor stimulating stem elongation in proteolytic and non-proteolytic signaling, and stimulating fertility in proteolytic GA signaling. GID1b plays the primary role in fertility, and a secondary role in elongation during non-proteolytic GA signaling. The stronger role of GID1b in non-proteolytic GA signaling may result from the fact that GID1b has higher affinity for DELLA protein than GID1a and GID1c.

摘要

赤霉素(GA)激素信号传导通过蛋白水解和非蛋白水解机制发生。GA与GA受体GID1(GA不敏感矮化1)结合,使GID1能够结合GA反应的负调节因子,即DELLA蛋白。在蛋白水解GA信号传导中,SLEEPY1(SLY1)F-box蛋白将GID1-GA-DELLA复合物中的DELLA蛋白靶向通过泛素-蛋白酶体途径进行降解。在GA无法将DELLA蛋白靶向降解的sly1突变体中的非蛋白水解GA信号传导,需要GA和GID1基因功能。基于gid1多个突变体与sly1 gid1突变体的比较,GID1a是在蛋白水解和非蛋白水解信号传导中刺激茎伸长以及在蛋白水解GA信号传导中刺激育性的主要GA受体。GID1b在育性中起主要作用,在非蛋白水解GA信号传导期间的伸长中起次要作用。GID1b在非蛋白水解GA信号传导中更强的作用可能是由于GID1b对DELLA蛋白的亲和力高于GID1a和GID1c。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/746c/4091331/2df6eaa57745/psb-9-e28030-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/746c/4091331/ab3eedbdc922/psb-9-e28030-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/746c/4091331/2df6eaa57745/psb-9-e28030-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/746c/4091331/ab3eedbdc922/psb-9-e28030-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/746c/4091331/2df6eaa57745/psb-9-e28030-g2.jpg

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