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Physical and genetic interactions of proteins required for asymmetric cell division in maize

Abstract

In Zea mays stomatal complex formation, pangloss (pan) and brick (brk) mutants have been identified that have aberrant subsidiary cell morphology due to abnormal polarization of the subsidiary mother cell (SMC). Current knowledge of SMC division signaling pathway involves PAN1, PAN2 and actin patch accumulation at the guard mother cell (GMC)-SMC contact site. PAN1 and PAN2 are inactive leucine rich repeat receptor-like kinases thought to be involved in signal transduction. BRK1, BRK2 and BRK3 are different components of the SCAR/WAVE complex that regulates an actin nucleator called Arp2/3 complex. In this study, the relationship between PAN and BRK were studied in regards to SMC polarization. Pan1 and Pan2 both interact genetically with Brk1 and Brk3, suggesting common roles in the SMC polarization-signaling cascade. Our previous model suggested BRK works downstream of PAN1 and PAN2, presumably as a promoter of the actin patch formation. However, in this study BRK1 appears to be upstream of PAN1, PAN2 and the actin patch, and is at least partially responsible for polarizing PAN1. I propose alternative roles for BRK in SMC polarization such as possible functions in vesicle trafficking and/or inhibition of receptor endocytosis

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