Formation of somatic embryos from non-germline cells is unique to higher plants and can be manipulated in a variety of species. Previous studies revealed that overexpression of several Arabidopsis genes, including WUS...Formation of somatic embryos from non-germline cells is unique to higher plants and can be manipulated in a variety of species. Previous studies revealed that overexpression of several Arabidopsis genes, including WUSCHEL （WUS）/PLANT GROWTH ACTIVATOR6 （PGA6）, BABY BOOM, LEAFY COTYLEDON1 （LEC1）, and LEC2, is able to cause vegetative-to-embryonic transition or the formation of somatic embryos. Here, we report that a gain-offunction mutation in the Arabidopsis PGA37 gene, encoding the MYBI18 transcription factor, induced vegetative-toembryonic transition, the formation of somatic embryos from root explants, and an elevated LEC1 expression level. Double mutant analysis showed that WUS was not required for induction of somatic embryos by PGA37/MYB118. In addition, overexpression of MYBll5, a homolog of PGA37/MYB118, caused a pga37-like phenotype. A myb118 myb115 double mutant did not show apparent developmental abnormalities. Collectively, these results suggest that PGA37/ MYB118 and MYB115 promote vegetative-to-embryonic transition, through a signaling pathway independent of WUS.展开更多
文摘Formation of somatic embryos from non-germline cells is unique to higher plants and can be manipulated in a variety of species. Previous studies revealed that overexpression of several Arabidopsis genes, including WUSCHEL （WUS）/PLANT GROWTH ACTIVATOR6 （PGA6）, BABY BOOM, LEAFY COTYLEDON1 （LEC1）, and LEC2, is able to cause vegetative-to-embryonic transition or the formation of somatic embryos. Here, we report that a gain-offunction mutation in the Arabidopsis PGA37 gene, encoding the MYBI18 transcription factor, induced vegetative-toembryonic transition, the formation of somatic embryos from root explants, and an elevated LEC1 expression level. Double mutant analysis showed that WUS was not required for induction of somatic embryos by PGA37/MYB118. In addition, overexpression of MYBll5, a homolog of PGA37/MYB118, caused a pga37-like phenotype. A myb118 myb115 double mutant did not show apparent developmental abnormalities. Collectively, these results suggest that PGA37/ MYB118 and MYB115 promote vegetative-to-embryonic transition, through a signaling pathway independent of WUS.
