During embryo development, the vascular precursors and ground tissue stem cells divide to renew themselves and produce the vascular tissue, endodermal cells, and cortical cells. However, the molecular mechanisms regulating division of these stem cells have remained largely elusive. In this study, we show that loss of function of SOMATIC EMBRYOGENESIS RECEPTOR-LIKE KINASE (SERK) genes results in aberrant embryo development. Fewer cortical, endodermal, and vascular cells are generated in the embryos of serk1 serk2 bak1 triple mutants. WUSCHEL-RELATED HOMEOBOX 5 (WOX5) is ectopically expressed in vascular cells of serk1 serk2 bak1 embryos. The first transverse division of vascular precursors in mid-globular embryos and second asymmetric division of ground tissue stem cells in early-heart embryos are abnormally altered to a longitudinal division. The embryo defects can be partially rescued by constitutively activated mitogen-activated protein kinase (MAPK) kinase kinase YODA (YDA) and MAPK kinase MKK5. Taken together, our results reveal that SERK-mediated signals regulate division patterns of vascular precursors and ground tissue stem cells, likely via the YDA-MKK4/5 cascade, during embryo development.

在胚胎发育期间，维管束前体和地面组织干细胞分裂以自我更新并产生维管组织，内胚层细胞和皮层细胞。然而，调节这些干细胞分裂的分子机制仍然很难捉摸。在这项研究中，我们表明，体细胞胚发生受体样激酶（SERK）基因功能的丧失会导致异常的胚胎发育。较少的皮质，内胚层和血管细胞在serk1 serk2 bak1三突变体的胚胎中产生。与WUSCHEL相关的HOMEOBOX 5（WOX5）在serk1 serk2 bak1的血管细胞中异位表达胚胎。球形前体中的血管前体的第一次横向分裂和早期心脏胚胎中的地面组织干细胞的第二次不对称分裂被异常地改变为纵向分裂。可以通过组成性激活的丝裂原激活的蛋白激酶（MAPK）激酶激酶YODA（YDA）和MAPK激酶MKK5来部分挽救胚胎缺陷。综上所述，我们的研究结果表明SERK介导的信号在胚胎发育过程中可能通过YDA-MKK4 / 5级联调节了血管前体和地面组织干细胞的分裂方式。