SAP130 and CSN1 interact and regulate male gametogenesis in Arabidopsis thaliana
SAP130 and CSN1 interact and regulate male gametogenesis in Arabidopsis thaliana
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DOI：
10.1007/s10265-021-01260-0
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发表时间：
2021-02-08
影响因子：
2.8
通讯作者：
Tsuge，Tomohiko
中科院分区：
文献类型：
--
作者：
Aki，Shiori S.;Yura，Kei;Tsuge，Tomohiko
COP9信号小体(CSN)是一个由8个不同亚基组成的核复合体，控制着拟南芥广泛的发育过程。海因。突变体的零等位基因表现出导致幼苗致死的多效性表型。到目前为止，一些部分互补的转基因植株在其相应的零突变等位基因中表达特定的CSN亚基，用于绕过幼苗致死并研究CSN在发育后期的调控。其中一个与CSN1亚基对应的转基因植物FUS6/CSN1-3-4积累了野生型CSN1水平，并在营养生长期表现出正常的植物结构。在这里，我们通过组织学分析表明，FUS6/CSN1-3-4植物在双细胞期表现出花粉发育的障碍。这一缺陷与在SAP130的RNAi植物中观察到的缺陷相同，后者编码多蛋白剪接因子SF3B的一个亚单位。我们进一步剖析了先前报道的CSN1与SAP130之间的相互作用，揭示了位于CSN1(CSN1NN)N-末端的大约100个氨基酸残基是这种相互作用所必需的。在电子结构模型中，CSN1NN可以朝着SAP130摆动，对接在其从结构中伸出的螺旋插入上。这些结果支持我们的模型，即CSN1通过其C-末端半部分嵌入CSN蛋白复合体，并通过其N-末端部分到达靶点。综上所述，这是第一次报道CSN1和SAP130在雄性配子发生过程中相同的功能丧失表型。因此，我们认为SAP130和CSN1协同调节雄性生殖器官的发育。
COP9 signalosome (CSN) is a nuclear complex composed of eight distinct subunits that governs vast developmental processes inArabidopsis thaliana(L.) Heynh. The null alleles ofcsnmutants display pleiotropic phenotypes that result in seedling lethality. To date, several partially complemented transgenic plants, expressing the particular CSN subunit in its corresponding null mutant allele, were utilized to bypass seedling lethality and investigate CSN regulation at later stages of development. One such transgenic plant corresponding to CSN1 subunit,fus6/CSN1-3-4, accumulates wild-type level of CSN1 and displays normal plant architecture at vegetative stage. Here we show through histological analyses thatfus6/CSN1-3-4plants display impairment of pollen development at the bicellular stage. This defect is identical to that observed in RNAi plants ofSAP130, encoding a subunit of the multiprotein splicing factor SF3b. We further dissected the previously reported interaction between CSN1 and SAP130, to reveal that approximately 100 amino-acid residues located at the N-terminal end of CSN1 (CSN1NN) were essential for this interaction. In silico structure modeling demonstrated that CSN1NN could swing out towards SAP130 to dock onto its Helical Insertion protruding from the structure. These results support our model that CSN1 embeds itself within CSN protein complex through its C-terminal half and reaches out to targets through its N-terminal portion of the protein. Taken together, this is the first report to document the identical loss-of-function phenotypes of CSN1 and SAP130 during male gametogenesis. Thus, we propose that SAP130 and CSN1 coordinately regulate development of male reproductive organs.