VENOSA4, a Human dNTPase SAMHD1 Homolog, Contributes to Chloroplast Development and Abiotic Stress Tolerance.,Plant Physiology

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VENOSA4, a Human dNTPase SAMHD1 Homolog, Contributes to Chloroplast Development and Abiotic Stress Tolerance.
Plant Physiology ( IF 6.5 ) Pub Date : 2019-12-02 , DOI: 10.1104/pp.19.01108
Duorong Xu ₁ , Dario Leister ₁ , Tatjana Kleine ₂

Affiliation

Chloroplast biogenesis depends on an extensive interplay between the nucleus, cytosol, and chloroplasts, involving regulatory nucleus-encoded chloroplast proteins, as well as nucleocytosolic photoreceptors such as phytochromes (phys) and other extrachloroplastic factors. However, this whole process is only partially understood. Here, we describe the role of VENOSA4 (VEN4) in chloroplast development and acclimation to adverse growth conditions. A 35S:VEN4-eGFP fusion protein localizes to the nucleus in Arabidopsis (Arabidopsis thaliana) protoplasts, and VEN4 homologs are present in a wide range of eukaryotes including humans, where the corresponding homolog (SAMHD1) cleaves dNTPs. Defective photosynthesis in ven4 seedlings results from reduced accumulation of photosynthetic proteins and appears to be caused by a reduction in the translational capacity of chloroplasts. The negative effect of the ven4 mutation on photosynthesis can be phenotypically suppressed by germinating seeds in the presence of excess dCTP or a pool of dNTPs, implying that VEN4, like human SAMHD1, is involved in dNTP catabolism. Moreover, VEN4 activity is also required for optimal responses to cold and salt stresses. In conclusion, our work emphasizes the importance of the nucleocytosolic compartment and the fine-tuning of dNTP levels for chloroplast translation and development.

中文翻译：

VENOSA4 是一种人类 dNTPase SAMHD1 同源物，有助于叶绿体发育和非生物胁迫耐受性。

叶绿体生物发生取决于细胞核、细胞质和叶绿体之间广泛的相互作用，涉及调节细胞核编码的叶绿体蛋白，以及核胞质光感受器，例如光敏色素 (phys) 和其他叶绿体外因子。然而，这整个过程仅被部分了解。在这里，我们描述了 VENOSA4 (VEN4) 在叶绿体发育和适应不利生长条件中的作用。 35S:VEN4-eGFP 融合蛋白定位于拟南芥 (Arabidopsis thaliana) 原生质体的细胞核，VEN4 同源物存在于包括人类在内的多种真核生物中，其中相应的同源物 (SAMHD1) 可裂解 dNTP。 ven4 幼苗的光合作用缺陷是由于光合蛋白积累减少造成的，并且似乎是由叶绿体翻译能力降低引起的。 ven4 突变对光合作用的负面影响可以在过量 dCTP 或 dNTP 库存在的情况下通过发芽种子在表型上受到抑制，这意味着 VEN4 与人类 SAMHD1 一样参与 dNTP 分解代谢。此外，VEN4 活性也是对冷和盐胁迫的最佳反应所必需的。总之，我们的工作强调了核胞质区室和 dNTP 水平微调对于叶绿体翻译和发育的重要性。

更新日期：2020-01-31

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