Zhang Shengchun, Zhang Daowei, Yang Chengwei
a Guangdong Key Lab of Biotechnology for Plant Development; College of Life Sciences; South China Normal University; Guangzhou, PR China.
Plant Signal Behav. 2014;9(9):e29709. doi: 10.4161/psb.29709.
Mitochondrial AtFtsH4 protease is one of four inner membrane-bound FtsH proteases in Arabidopsis. We found that the loss of AtFtsH4 regulates Arabidopsis development and architecture by mediating the peroxidase-dependent interplay between hydrogen peroxide (H2O2) and auxin homeostasis. These morphological changes were correlated with elevated levels of both hydrogen peroxide and peroxidases, which suggested that ftsh4-4 plant was related to the oxidative stress, and that the architecture was caused by the auxin homeostasis perturbation. This view was supported by the expression levels of several auxin signaling genes and auxin binding and transport genes were decreased significantly in ftsh4-4 plants. Taken together, our data published in the May issue of Molecular Plant suggests a link between the lack of AtFtsH4 protease, oxidative stress,s and auxin homeostasis to regulate plant growth and development. However, the detail molecular mechanisms of AtFtSH4 regulating oxidation stress and auxin homeostasis is unclear. Here, we present evidence that the high level accumulated of H2O2 in ftsh4-4 may correlates with the decreased mitochondrial respiration genes. We also showed that the decreased auxin level and auxin transport may caused by the inhibition of mitochondrial respiratory chain complexes.
线粒体AtFtsH4蛋白酶是拟南芥中四种内膜结合型FtsH蛋白酶之一。我们发现，AtFtsH4的缺失通过介导过氧化氢（H2O2）和生长素稳态之间依赖过氧化物酶的相互作用来调节拟南芥的发育和结构。这些形态变化与过氧化氢和过氧化物酶水平的升高相关，这表明ftsh4 - 4植株与氧化应激有关，且其结构是由生长素稳态扰动引起的。这一观点得到了ftsh4 - 4植株中几个生长素信号基因以及生长素结合和转运基因表达水平显著降低的支持。综合来看，我们发表在《分子植物》五月刊上的数据表明，AtFtsH4蛋白酶的缺失、氧化应激和生长素稳态之间存在联系，共同调节植物生长发育。然而，AtFtSH4调节氧化应激和生长素稳态的具体分子机制尚不清楚。在此，我们提供证据表明，ftsh4 - 4中H2O2的高水平积累可能与线粒体呼吸基因的减少有关。我们还表明，生长素水平和生长素运输的降低可能是由线粒体呼吸链复合物的抑制引起的。
