抄録
In Arabidopsis cytokinin (CK)-signaling is mediated by a multi-step phosphorelay, which is comprised of histidine kinases (AHKs), phosphotransfers (AHPs) and response regulators (ARRs). Recently, we demonstrated that AHK2, AHK3 and AHK4 act as negative regulators in salt stress response, because disruption of these genes resulted in increased tolerance to salt stress. The AHKs were expected to act through one or more AHPs and ARRs, which are their downstream components in CK-phosphorelay, in salt stress response. To elucidate the regulatory role of CK-phosphorelay in salt stress response, we have carried out systematic functional studies of the AHPs and type-B ARRs by loss-of-function approaches. We have identified several ahp and type-B arr mutants that showed increased salt tolerance, suggesting that these AHPs and ARRs act as negative regulators in salt stress response. We will discuss the regulatory functions of these AHP and type-B ARR genes in response to salt stress. Our data will provide better insight into the complex stress signaling pathway regulated by the CK-phosphorelay.
