受体激酶ZAR1与SERKs和SSP蛋白相互协调共同调控合子的不对称分裂和分裂后子细胞的细胞命运

Asymmetric division of zygote is critical for pattern formation during early embryogenesis in plants and animals. It requires integration of the intrinsic and extrinsic cues prior to and/or after fertilization. How these cues are translated into developmental signals is poorly understood. Previously, we identified an Arabidopsis mutant, zygotic arrest 1 (zar1), in which zygote asymmetric division and the cell fate of its daughter cells were impaired. ZAR1 encodes a member of leucine rich repeat kinase family. ZAR1 is specifically expressed in central cell, egg cell and synergids in the mature embryo sac. After fertilization, ZAR1 is accumulated in zygote and endosperm. We demonstrated that ZAR1 physically interacts with Calmodulin and the heterotrimeric G protein Gβ. The disruption of ZAR1 and AGB1 results in a short basal cell and an apical cell with basal cell fate. It suggest that ZAR1 functions as a membrane integrator for extrinsic cues, Ca2+ signal and G protein signaling to regulate the division of zygote and the cell fate of its daughter cells. Here we found ZAR1 interplays with SSP in vitro. The deletion of ZAR1 and SSP leads to an equal basal cell and an apical cell with the symmetric division of zygote. As we known, SSP regulated the asymmetric division of zygote in the SSP/YODA MAPK cascade signal pathway. It is well worthy to investigate the link between ZAR1/AGB1 pathway and YODA MAPK kinase cascade signaling. We will clarify the relationship among ZAR1, SSP and AGB1(Gβ) by the means of genetic and molecular biology. These discoveries will pave an avenue for elucidating the component of ZAR1 signal and its functions in orchestrating the asymmetric division of zygote and cell fate of its daughter cells.

合子的不对称分裂在动、植物早期胚胎模式建成中发挥着至关重要的作用。来自受精前、后细胞内在和外部的各种发育信号，共同调控合子的不对称分裂。我们获得拟南芥zar1-2，产生合子对称分裂和顶细胞带有基细胞特征的异常表型，ZAR1基因受精前在中央细胞、卵细胞和助细胞中特异表达，受精后在合子和胚乳中特异表达。ZAR1与Ca2+/CaM和G蛋白亚单位Gβ直接相互作用。Gβ突变产生类似zar1-2的合子和顶细胞异常表型。证实ZAR1结合Ca2+和异源三聚体G蛋白，共同调控合子的发育。ZAR1体外可以与SSP发生相互作用，双突变zar1-2/ssp产生合子对称分裂的异常表型。我们通过细胞生化技术研究SSP、ZAR1和AGB1(Gβ）三者之间的关系，以期阐明ZAR1/AGB1和SSP/YODA信号途径的联系，研究调控合子不对称分裂和分裂后顶、基细胞命运的分子机制。