The Arabidopsis Receptor Kinase ZAR1 Is Required for Zygote Asymmetric Division and Its Daughter Cell Fate.
The Arabidopsis Receptor Kinase ZAR1 Is Required for Zygote Asymmetric Division and Its Daughter Cell Fate.
复制标题
DOI：
10.1371/journal.pgen.1005933
复制
发表时间：
2016-03
期刊：
影响因子：
4.5
通讯作者：
Yang WC
中科院分区：
文献类型：
--
作者：
Yu TY;Shi DQ;Jia PF;Tang J;Li HJ;Liu J;Yang WC
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. Here through genetic screen for mutations affecting early embryogenesis, 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 the RLK/Pelle kinase family. We demonstrated that ZAR1 physically interacts with Calmodulin and the heterotrimeric G protein Gβ, and ZAR1 kinase is activated by their binding as well. ZAR1 is specifically expressed micropylarly in the embryo sac at eight-nucleate stage and then in central cell, egg cell and synergids in the mature embryo sac. After fertilization, ZAR1 is accumulated in zygote and endosperm. The disruption of ZAR1 and AGB1 results in short basal cell and an apical cell with basal cell fate. These data 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 in Arabidopsis. Flowering plants are featured as double fertilization, a process that the egg cell and the central cell of embryo sac fuse with a sperm and give rise to a diploid zygote and a triploid primary endosperm cell, respectively. The zygote develops into embryo after cell division and differentiation, and starts a new trip of next generation. Meanwhile, the primary endosperm cell proceeds nuclear division to generate a syncytium and develops into endosperm after cellularization. Embryo development initiates from asymmetric division of zygote. A small apical cell and a long basal cell are produced after the first zygotic division, which establishes the pattern of an early embryo. To unveil the molecular mechanism controlling zygote asymmetric division, we screened our Ac/Ds insertion lines for mutations controlling early embryogenesis, one of the mutations zygotic arrest 1 (zar1) was reported here. In zar1, zygote was either arrested after elongation or displayed symmetric division. The mutation also had a slight impact on the apical- and basal-cell fates manifested by the mis-expression of the cell-lineage specific markers. ZAR1 encodes a member of the RLK/Pelle kinase family, and interacts physically with Calmodulin and the heterotrimeric G protein Gβ, both in vitro and in vivo. These data suggest that ZAR1 might act as an integrator for intracellular Ca2+ and heterotrimeric G protein signaling with extracellular signals during early zygote development. Interestingly, complete loss of Gβ or ZAR1 function displayed very weak phenotype. This suggests that there might be genetic redundancy and plasticity during early embryogenesis. More studies are needed to dissect the complexity of early embryo development in plants.
