Knox homologs shoot meristemless (STM) and KNAT6 are epistatic to CLAVATA3 (CLV3) during shoot meristem development in Arabidopsis thaliana

In Arabidopsis, the genes SHOOT MERISTEMLESS (STM) and CLAVATA3 (CLV3) antagonistically regulate shoot meristem development. STM is essential for both development and maintenance of the meristem, as stm mutants fail to develop a shoot meristem. CLV3, on the other hand, negatively regulates meristem proliferation, and clv3 mutants possess an enlarged shoot meristem. Genetic interaction studies revealed that stm and clv3 dominantly suppress each other's phenotypes. STM works in conjunction with its closely related homologue KNOTTED1-LIKE HOMEOBOX GENE 6 (KNAT6) to promote meristem development and organ separation, as stm knat6 double mutants fail to form shoot meristem and produce a fused cotyledon.In this study, we show that clv3 fails to promote shoot meristem formation in stm-1 background if we also remove KNAT6. stm-1 knat6 clv3 triple mutants result in shoot meristem termination and produce fused cotyledons similar to stm knat6 double mutant. Notably, the stm-1 knat6 and stm-1 knat6 clv3 alleles lack tissue in the presumed region of SAM that is a novel phenotype reported in Arabidopsis mutants. stm-1 knat6 clv3 also showed reduced inflorescence size as compared to clv3 single or stm clv3 double mutants.In contrast to previously published data, these data suggest that STM and KNAT6 are redundantly required for the vegetative SAM, but insufficient for the inflorescence meristem.