Interaction between RNA helicase ROOT INITIATION DEFECTIVE 1 and GAMETOPHYTIC FACTOR 1 is involved in female gametophyte development in Arabidopsis.

Interaction between RNA helicase ROOT INITIATION DEFECTIVE 1 and GAMETOPHYTIC FACTOR 1 is involved in female gametophyte development in Arabidopsis.
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RNA解旋酶根启动缺陷1和配子体因子1之间的相互作用参与拟南芥雌配子体发育

DOI:
10.1093/jxb/erw341
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发表时间:
2016-10
影响因子:
6.9
通讯作者:
Zhang XS
Zhang XS
中科院分区:
生物学1区
文献类型:
--
作者:
Zhu DZ;Zhao XF;Liu CZ;Ma FF;Wang F;Gao XQ;Zhang XS

文献摘要

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RID1与GFA1相互作用,指导和调节拟南芥雌配子体发育所需基因的剪接和表达。根起始缺陷1(RID1)是拟南芥Deah/RHA RNA解旋酶。它在下胚轴去分化、新生分生组织的形成和成熟雌配子体(FG)的细胞特化过程中发挥作用。然而,目前还不清楚RID1是如何调控FG的发育的。在这项研究中,我们观察到RID1的突变破坏了发育的同步性,并延缓了FG的发展。RID1具有RNA解旋酶活性,倾向于3‘-5’方向解离双链RNA。此外,我们还发现RID1与GAMETOPHYTIC factor1(GFA1)相互作用,GFA1是剪接体成分U5小核核糖核蛋白(SnRNP)颗粒的完整蛋白。特异性RID1氨基酸(Y266F和T267I)的替代抑制了与GFA1的相互作用。此外,突变的RID1不能补充Rid1突变体的种子败育表型。Rid1和gfa1突变体在前mRNA剪接和FG发育相关基因表达下调方面表现出相似的异常。我们的结果表明,RID1和U5 SnRNP复合体之间的相互作用调节着FG发育所需基因的必要的前mRNA剪接。这项研究为FG发育过程的潜在机制提供了新的信息。
RID1 interacts with GFA1 to direct and regulate the splicing and expression of the genes required for female gametophyte development in Arabidopsis. ROOT INITIATION DEFECTIVE 1 (RID1) is an Arabidopsis DEAH/RHA RNA helicase. It functions in hypocotyl de-differentiation, de novo meristem formation, and cell specification of the mature female gametophyte (FG). However, it is unclear how RID1 regulates FG development. In this study, we observed that mutations to RID1 disrupted the developmental synchrony and retarded the progression of FG development. RID1 exhibited RNA helicase activity, with a preference for unwinding double-stranded RNA in the 3′ to 5′ direction. Furthermore, we found that RID1 interacts with GAMETOPHYTIC FACTOR 1 (GFA1), which is an integral protein of the spliceosome component U5 small nuclear ribonucleoprotein (snRNP) particle. Substitution of specific RID1 amino acids (Y266F and T267I) inhibited the interaction with GFA1. In addition, the mutated RID1 could not complement the seed-abortion phenotype of the rid1 mutant. The rid1 and gfa1 mutants exhibited similar abnormalities in pre-mRNA splicing and down-regulated expression of some genes involved in FG development. Our results suggest that an interaction between RID1 and the U5 snRNP complex regulates essential pre-mRNA splicing of the genes required for FG development. This study provides new information regarding the mechanism underlying the FG developmental process.