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        The F-box Protein KIB1 Mediates Brassinosteroid-Induced Inactivation and Degradation of GSK3-like Kinases in <i>Arabidopsis</i>

        Zhu, Jia-Ying,Li, Yuyao,Cao, Dong-Mei,Yang, Hongjuan,Oh, Eunkyoo,Bi, Yang,Zhu, Shengwei,Wang, Zhi-Yong Elsevier 2017 Molecular cell Vol.66 No.5

        <P><B>Summary</B></P> <P>The glycogen synthase kinase-3 (GSK3) family kinases are central cellular regulators highly conserved in all eukaryotes. In <I>Arabidopsis</I>, the GSK3-like kinase BIN2 phosphorylates a range of proteins to control broad developmental processes, and BIN2 is degraded through unknown mechanism upon receptor kinase-mediated brassinosteroid (BR) signaling. Here we identify KIB1 as an F-box E3 ubiquitin ligase that promotes the degradation of BIN2 while blocking its substrate access. Loss-of-function mutations of KIB1 and its homologs abolished BR-induced BIN2 degradation and caused severe BR-insensitive phenotypes. KIB1 directly interacted with BIN2 in a BR-dependent manner and promoted BIN2 ubiquitination in vitro. Expression of an F-box-truncated KIB1 caused BIN2 accumulation but dephosphorylation of its substrate BZR1 and activation of BR responses because KIB1 blocked BIN2 binding to BZR1. Our study demonstrates that KIB1 plays an essential role in BR signaling by inhibiting BIN2 through dual mechanisms of blocking substrate access and promoting degradation.</P> <P><B>Highlights</B></P> <P> <UL> <LI> KIB1 is an essential positive regulator in brassinosteroid signaling </LI> <LI> KIB1 mediates BR-induced ubiquitination and degradation of GSK3 kinase BIN2 </LI> <LI> KIB1 binding to BIN2 prevents BIN2-substrate interaction and promotes BIN2 degradation </LI> </UL> </P> <P><B>Graphical Abstract</B></P> <P>[DISPLAY OMISSION]</P>

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        The GntR-Type Regulators GtrA and GtrB Affect Cell Growth and Nodulation of Sinorhizobium meliloti

        Yi Wang,Ai-Min Chen,Ai-Yuan Yu,Li Luo,Guan-Qiao Yu,Jia-Bi Zhu,Yan-Zhang Wang 한국미생물학회 2008 The journal of microbiology Vol.46 No.2

        GntR-type transcriptional regulators are involved in the regulation of various biological processes in bacteria, but little is known about their functions in Sinorhizobium meliloti. Here, we identified two GntR-type transcriptional regulator genes, gtrA and gtrB, from S. meliloti strain 1021. Both the gtrA1 mutant and the gtrB1 mutant had lower growth rates and maximal cell yields on rich and minimal media, as well as lower cell motility on swimming plates, than did the wild-type strain. Both mutants were also symbiotically deficient. Alfalfa plants inoculated with wild-type strain 1021 formed pink elongated nodules on primary roots. In contrast, the plants inoculated with the gtrA1 and gtrB1 mutants formed relatively smaller, round, light pink nodules mainly on lateral roots. During the first 3~4 weeks post-inoculation, the plants inoculated with the gtrA1 and gtrB1 mutants were apparently stunted, with lower levels of nitrogenase activity, but there was a remarkable increase in the number of nodules compared to those inoculated with the wild-type strain. Moreover, the gtrA1 and gtrB1 mutants not only showed delayed nodulation, but also showed markedly reduced nodulation competition. These results demonstrated that both GtrA and GtrB affect cell growth and effective symbiosis of S. meliloti. Our work provides new insight into the functions of GntR-like transcriptional regulators.

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