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Abstract:
In flowering plants, many asymmetric cell divisions are controlled by a MAP kinase signaling pathway including the MAP3K YODA. In the early Arabidopsis embryo, this YODA-dependent pathway is activated by two distinct mechanisms: by canonical activation of an evolutionarily conserved receptor complex and by the Brassicaceae-specific membrane-associated protein SHORT SUSPENSOR that activates YODA independent of receptor activation. We will present genetic data that clearly identifies the receptor kinase that functions upstream of YODA in the early embryo. Furthermore, we will give mechanistic insight in the evolution of this receptor kinase/MAP kinase signaling pathway as well as the regulation of YODA signaling on a molecular level. In addition, we will discuss the distinct parental
contributions to embryonic patterning and their possible selective benefits.
