Cotton GhCKI regulates anther abortion by delaying tapetum PCD via the GLU-ABA-ROS signalling pathway

Working group session: 
Functional Genomics
Presentation type: 
oral
Authors: 
Min, Ling; Zhang, Xianlong
Presenter: 
Zhang, Xianlong
Correspondent: 
Zhang, Xianlong
Abstract: 
Infertility of anthers under high temperature (HT) has become a critical factor in yield loss in cotton. Previous studies showed altered carbohydrate metabolism or disrupted tapetal cell programmed cell death (PCD) underlie anther sterility. Through large-scale expression profile sequencing we studied the effect of HT on cotton anther development and found that the GhCKI gene, highly homologous with casein kinase I (CKI), was induced by HT in a HT-sensitive cotton line. Our studies showed GhCKI causes glucose (GLU) accumulation in early-stage anthers by inactivating starch synthase via phosphorylation. Subsequent feedback inhibition of glucose assimilation and induction of starch synthesis cause a deficiency in glucose in late-stage anthers. The early accumulation of glucose also promotes excessive amounts of abscisic acid (ABA) in early anthers and alters the balance of reactive oxygen species (ROS) scavenging and accumulation in late anthers, causing delayed PCD in the tapetum leading to anther indehiscence.