SCREAM to stop SPEECHLESS

Abstract

During stomatal development, protodermal cells differentiate into meristemoid mother cells, which undergo a limited number of asymmetric cell divisions that each produce a smaller meristemoid and a larger stomatal-lineage ground cell. The final meristemoid further differentiates into a guard mother cell, which divides symmetrically to produce two guard cells. The asymmetric divisions of the meristemoid mother cell are initiated by SPCH, whereas MUTE is required for termination of asymmetric divisions and further differentiation of the meristemoid into the guard mother cell. Finally, FAMA is required for symmetric division of the guard mother cell. SPCH, MUTE and FAMA can all form heterodimers with SCREAM; however, the specific role of SCREAM in stomatal development is less clear.

The researchers investigate stomatal development in scrm mutants and find that differentiation of stomatal-lineage cells into guard cells is inhibited. Although the number of asymmetric cell divisions in scrm mutants differs between developmental stages compared with the wild type, lack of SCRM generally leads to excessive asymmetric cell divisions of meristemoids. As overexpression of SCRM leads to increased stomatal-lineage density but not stomatal density, it seems that SCRM is required both for the initiation and termination of asymmetric cell division at different stages. Transcription of SPCH and known SPCH targets is enhanced in scrm mutants, and indeed SCRM can directly bind and repress the SPCH promoter. It is further shown that SPCH is epistatic to SCRM and that downregulation of SPCH expression in the scrm background can partially suppress the excessive asymmetric cell divisions, suggesting that this phenotype can be at least partially attributed to upregulation of SPCH in the scrm mutant. Overexpression of SCRM in the mute background leads to fewer asymmetric cell divisions than in mute alone, and MUTE does not bind to the SPCH promoter in vivo, pointing to a role for SCRM in the termination of asymmetric cell divisions that is independent of MUTE. As it was shown before that SPCH can also be inhibited by non-cell autonomous patterning signals, it is tempting to speculate that relative quantities of SPCH and SCRM may determine the initiation or termination of asymmetric cell division.