Symmetrica is involved in leaf development and stem cell fate

ASYMMETRIC LEAVES1 (AS1) encodes a MYB transcription factor that is expressed in lateral organs of Arabidopsis where it excludes expression of meristem promoting know genes. This is unlikely to be the only function of AS1 as reducing knox expression does not suppress the as1 mutant phenotype. To identify additional targets of AS1, gain-of-function and loss-of-function mutant screens were used to identify modifiers of the as1 mutant phenotype. A gain of function mutation in the PTL gene was isolated as a potential suppressor of the as1 mutant phenotype in petals. Further genetic analysis suggested that AS1 and PTL are unlikely to act in same pathway. symmetrica (sym), a complete suppressor of as1, was isolated in loss-of-function screens. Expression analysis of knox expression in lateral organs of sym mutants suggests that SYM is required for knox upregulation in as1 mutant lateral organs. AS2, which is thought to act in a similar position in development to AS1 also appeared to interact with SYM as as2 mutants were also suppressed in its absence. Triple mutant analysis indicated that SYM may work in a similar position in development to SE, a previously described partial suppresser of as1. In the absence of the knox gene STM, formation of a functional SAM during embryogenesis is prevented due to ectopic expression of AS1 and genes that specify lateral organ fate throughout the apex. However, as1-1 stm-1 double mutants form a functional SAM as lateral organ fate signals are reduced due to the lack of AS1. The SAM of as1-1 sym stm-1 triple mutants is arrested, indicating a redundant role for SYM in meristem function. sym also modified mutants at the PNH locus, suggesting an interaction with the post translational gene silencing machinery. SYM was mapped to an interval of 120 Mb linked to AS1 on the long arm of chromosome 2.