Overexpression of AtCHX24, a member of the cation/H⁺ exchangers, accelerates leaf senescence in Arabidopsis thaliana

Abstract

Leaf senescence, the final stage of leaf development, occurs in an age-dependent manner but can be finely regulated by other developmental and environmental factors. Despite the discovery of many genes involved in leaf senescence, the molecular genetic mechanisms of leaf senescence are still unclear. In this study, an activation-tagging based suppressor screen was performed to identify Arabidopsis genes that could suppress the delayed leaf senescence phenotypes of oresara9-1 (ore9-1) when overexpressed. The suppressor1 of ore9 dominant (sor1-D) was caused by the overexpression of AtCHX24, a putative cation/H(+) exchanger. The sor1-D mutation suppressed the phenotypes of ore9 in age-dependent and dark-induced senescence. Furthermore, the sor1-D mutation restored the delayed senescence phenotypes of ore1 and ore3. The sor1-D mutant also exhibited increased sensitivity to pH changes during dark-induced leaf senescence. Collectively, overexpression of AtCHX24 results in accelerated leaf senescence and these results suggest that AtCHX24 plays an important role in regulating leaf senescence.