Abstract
InArabidopsis,the genes SHOOT MERISTEMLESS(STM) andCLAVATA3 (CLV3) antagonistically regulate shoot meristem development.STMis essential for both development and maintenance of the meristem, asstmmutants fail to develop a shoot meristem.CLV3, on the other hand, negatively regulates meristem proliferation, andclv3mutants possess an enlarged shoot meristem. Genetic interaction studies revealed thatstmandclv3 dominantly suppress each other's phenotypes. STM works in conjunction withits closely related homologue KNOTTED1-LIKE HOMEOBOX GENE 6 (KNAT6)to promote meristem development and organ separation, asstmknat6double mutants fail to form shoot meristem and produce a fused cotyledon. In this study, we show thatclv3fails topromoteshoot meristem formation instm-1background if we also remove KNAT6.stm-1knat6 clv3triple mutants result in shoot meristem termination and produce fused cotyledons similar tostmknat6double 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-1knat6 clv3also showed reduced inflorescence size as compared toclv3single orstmclv3double mutants. In contrast to previously published data, these data suggest thatSTM and KNAT6 are redundantly required for the vegetative SAM, but insufficient for the inflorescence meristem.
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