The mitochondrial protease AtFTSH4 safeguards Arabidopsis shoot apical meristem function.
The mitochondrial protease AtFTSH4 safeguards Arabidopsis shoot apical meristem function.
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DOI：
10.1038/srep28315
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发表时间：
2016-06-20
影响因子：
4.6
通讯作者：
Janska H
中科院分区：
文献类型：
--
作者：
Dolzblasz A;Smakowska E;Gola EM;Sokołowska K;Kicia M;Janska H
顶端分生组织(SAM)保证了植物的持续生长和器官发生。在LD30 °C中，缺乏AtFTSH4的植物表现出一种令人费解的提前终止SAM的表型。AtFTSH4是一种依赖于ATP的线粒体蛋白酶，可以抵消内部氧化胁迫的积累。我们的目标是阐明将AtFTSH4与SAM抑制联系起来的潜在的细胞和分子过程。我们研究了AtFTSH4的表达、内部氧化应激积累和SAM形态。直接在SAM中，我们使用WUS/CLV3表达分析了过氧化氢积累、线粒体行为和干细胞的身份。AtFTSH4在增殖期组织中表达，特别是在生殖期。在突变体SAM中，内部氧化应激主要在30 °C积累，失去了分生组织的命运。这一进程是循序渐进的，分阶段进行。分生组织过早终止与SAM区扩张有关，线粒体在SAM区失去功能。所有这些影响都破坏了干细胞的身份。在ftsh4突变体中SAM的终止既是由随时间/年龄的内部氧化应激积累引起的，也是由AtFTSH4在开花转变周围的组织特异性作用引起的。依赖于AtFTSH4，在SAM内维持线粒体功能，对于在整个发育过程中保持干细胞活性至关重要。
The shoot apical meristem (SAM) ensures continuous plant growth and organogenesis. In LD 30 °C, plants lacking AtFTSH4, an ATP-dependent mitochondrial protease that counteracts accumulation of internal oxidative stress, exhibit a puzzling phenotype of premature SAM termination. We aimed to elucidate the underlying cellular and molecular processes that link AtFTSH4 with SAM arrest. We studied AtFTSH4 expression, internal oxidative stress accumulation, and SAM morphology. Directly in the SAM we analysed H2O2 accumulation, mitochondria behaviour, and identity of stem cells using WUS/CLV3 expression. AtFTSH4 was expressed in proliferating tissues, particularly during the reproductive phase. In the mutant, SAM, in which internal oxidative stress accumulates predominantly at 30 °C, lost its meristematic fate. This process was progressive and stage-specific. Premature meristem termination was associated with an expansion in SAM area, where mitochondria lost their functionality. All these effects destabilised the identity of the stem cells. SAM termination in ftsh4 mutants is caused both by internal oxidative stress accumulation with time/age and by the tissue-specific role of AtFTSH4 around the flowering transition. Maintaining mitochondria functionality within the SAM, dependent on AtFTSH4, is vital to preserving stem cell activity throughout development.