Arabidopsis Histidine Kinase CKI1 Acts Upstream of HISTIDINE PHOSPHOTRANSFER PROTEINS to Regulate Female Gametophyte Development and Vegetative Growth
Yan Deng,Haili Dong,Jinye Mu,Bo Ren,Binglian Zheng,Zhendong Ji,Wei-Cai Yang,Yan Liang,and Jianru Zuo

Plant Cell
DOI:10.1105/tpc.108.065128

Abstract

Cytokinin signaling is mediated by a multiple-step phosphorelay.Key components of the phosphorelay consist of the histidinekinase (HK)-type receptors, histidine phosphotransfer proteins(HP), and response regulators (RRs). Whereas overexpressionof a nonreceptor-type HK gene CYTOKININ-INDEPENDENT1 (CKI1)activates cytokinin signaling by an unknown mechanism, mutationsin CKI1 cause female gametophytic lethality. However, the functionof CKI1 in cytokinin signaling remains unclear. Here, we characterizea mutant allele, cki1-8, that can be transmitted through femalegametophytes with low frequency (0.17%). We have recovered viablehomozygous cki1-8 mutant plants that grow larger than wild-typeplants, show defective megagametogenesis and rarely set enlargedseeds. We found that CKI1 acts upstream of AHP (ArabidopsisHP) genes, independently of cytokinin receptor genes. Consistently,an ahp1,2-2,3,4,5 quintuple mutant, which contains an ahp2-2null mutant allele, exhibits severe defects in megagametogenesis,with a transmission efficiency of <3.45% through female gametophytes.Rarely recovered ahp1,2-2,3,4,5 quintuple mutants are seedlinglethal. Finally, the female gametophytic lethal phenotype ofcki1-5 (a null mutant) can be partially rescued by IPT8 or ARR1(a type-B Arabidopsis RR) driven by a CKI1 promoter. These resultsdefine a genetic pathway consisting of CKI1, AHPs, and type-BARRs in the regulation of female gametophyte development andvegetative growth.