Cotton GhCKI disrupts normal male reproduction by delaying tapetum programmed cell death via inactivating starch synthase

Abstract

Anther infertility under high temperature (HT) conditions has become a critical factor contributing to yield loss in cotton. Using large-scale expression profile sequencing, we studied the effect of HT on cotton anther development. Our analysis revealed that altered carbohydrate metabolism or disrupted tapetal programmed cell death (PCD) underlie anther sterility. The Gossypium hirsutum casein kinase I (GhCKI) gene, which encodes a homolog of casein kinase I (CKI), was induced in a HT-sensitive cotton line after exposure to HT. As mammalian homologs of GhCKI are involved in the inactivation of glycogen synthase and the regulation of apoptosis, GhCKI should be considered a target gene for improving anther fertility under HT conditions. Our studies suggest that GhCKI exhibits starch synthase kinase activity, increases glucose (Glc) content in early stage buds and activates the accumulation of abscisic acid (ABA), thereby disturbing the balance of reactive oxygen species (ROS) and eventually disrupting tapetal PCD, leading to anther abortion or indehiscence. These results indicate that GhCKI may be a key regulator of tapetal PCD and anther dehiscence, with the potential to facilitate the regulation of HT tolerance in crops.