R1R2R3-Myb proteins positively regulate cytokinesis through activation of KNOLLE transcription in Arabidopsis thaliana

R1R2R3-Myb proteins positively regulate cytokinesis through activation of KNOLLE transcription in Arabidopsis thaliana
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DOI:
10.1242/dev.02801
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发表时间:
2007-03-15
期刊:
影响因子:
4.6
通讯作者:
Ito, Masaki
Ito, Masaki
中科院分区:
生物学2区
文献类型:
--
作者:
Haga, Nozomi;Kato, Kiichi;Ito, Masaki

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烟草细胞中G2/M期特异性基因转录由R1 R2 R3-Myb转录激活因子NtmybA 1和NtmybA 2介导,它们与有丝分裂特异性激活因子(MSA)元件结合。我们在这里表明,两个结构相关的基因,MYB 3R 1和MYB 3R 4,编码NtmybA 1和NtmybA 2的同源物,发挥了部分冗余的作用,积极调节拟南芥胞质分裂。myb 3r 1和myb 3r 4双突变体通常不能完成胞质分裂,导致多核细胞在不同组织中具有有间隙的细胞壁和细胞壁残端。这些缺陷与几个G2/M期特异性基因的转录水平的选择性降低相关,这些基因包括B2型细胞周期蛋白(CYCB 2)、CDC 20.1和诺勒(KN)。这些基因在其启动子中含有MSA样基序,并且在烟草细胞中的瞬时表达测定中被MYB 3R 4激活。KN基因编码一种对细胞板形成必不可少的多核分裂特异性突触融合蛋白。myb 3r 1和myb 3r 4双突变体的胞质分裂缺陷部分拯救KN基因表达从异源启动子。此外,kn杂合突变增强了MYB 3R 1和MYB 3R 4基因杂合或纯合突变引起的胞质分裂缺陷。我们的研究结果表明,一对结构相关的R1 R2 R3-Myb转录因子可能正调控胞质分裂主要通过转录激活KN基因。
G2/M phase-specific gene transcription in tobacco cells is mediated by R1R2R3-Myb transcriptional activators, NtmybA1 and NtmybA2, which bind to mitosis-specific activator (MSA) elements. We show here that two structurally related genes, MYB3R1 and MYB3R4, which encode homologs of NtmybA1 and NtmybA2, play a partially redundant role in positively regulating cytokinesis in Arabidopsis thaliana. The myb3r1 myb3r4 double mutant often fails to complete cytokinesis, resulting in multinucleate cells with gapped walls and cell wall stubs in diverse tissues. These defects correlate with the selective reduction of transcript levels of several G2/M phase-specific genes, which include B2-type cyclin (CYCB2), CDC20.1 and KNOLLE (KN). These genes contain MSA-like motifs in their promoters and were activated by MYB3R4 in transient expression assays in tobacco cells. The KN gene encodes a cytokinesis-specific syntaxin that is essential for cell plate formation. The cytokinesis defects of myb3r1 myb3r4 double mutants were partially rescued by KN gene expression from heterologous promoters. In addition, a kn heterozygous mutation enhanced cytokinesis defects resulting from heterozygous or homozygous mutations in the MYB3R1 and MYB3R4 genes. Our results suggest that a pair of structurally related R1R2R3-Myb transcription factors may positively regulate cytokinesis mainly through transcriptional activation of the KN gene.