Department of Biological Science, Chungnam National University, Daejeon 305-764, Republic of Korea.
Plant Sci. 2012 Feb;183:175-82. doi: 10.1016/j.plantsci.2011.08.008. Epub 2011 Aug 25.
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.
叶片衰老，即叶片发育的最后阶段，是一种依赖于年龄的过程，但可以被其他发育和环境因素精细调节。尽管已经发现了许多参与叶片衰老的基因，但叶片衰老的分子遗传机制仍不清楚。在这项研究中，我们进行了基于激活标签的抑制子筛选，以鉴定当过度表达时可以抑制 oresara9-1（ore9-1）延迟叶片衰老表型的拟南芥基因。oresara9 显性抑制子 1（sor1-D）是由于拟南芥 AtCHX24 的过表达引起的，AtCHX24 是一种假定的阳离子/H(+) 交换蛋白。sor1-D 突变抑制了 ore9 在年龄依赖和黑暗诱导衰老中的表型。此外，sor1-D 突变恢复了 ore1 和 ore3 的延迟衰老表型。sor1-D 突变体在黑暗诱导的叶片衰老过程中对 pH 值变化的敏感性也增加了。总之，AtCHX24 的过表达导致叶片衰老加速，这些结果表明 AtCHX24 在调节叶片衰老中起着重要作用。
