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DnmA和FisA介导线粒体和过氧化物酶体分裂,并调节线粒体功能、活性氧生成及(此处原文未完整给出的某个生物体的)发育。

DnmA and FisA Mediate Mitochondria and Peroxisome Fission, and Regulate Mitochondrial Function, ROS Production and Development in .

作者信息

Garrido-Bazán Verónica, Pardo Juan Pablo, Aguirre Jesús

机构信息

Departamento de Biología Celular y del Desarrollo, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico.

Posgrado en Ciencias Biológicas, Unidad de Posgrado, Universidad Nacional Autónoma de México (UNAM), Mexico City, Mexico.

出版信息

Front Microbiol. 2020 May 4;11:837. doi: 10.3389/fmicb.2020.00837. eCollection 2020.

Abstract

The dynamin-like protein Drp1 and its receptor Fis-1 are required for mitochondria and peroxisome fission in animal and yeast cells. Here, we show that in the fungus the lack of Drp1 and Fis-1 homologs DnmA and FisA has strong developmental defects, leading to a notable decrease in hyphal growth and asexual and sexual sporulation, with some of these defects being aggravated or partially remediated by different carbon sources. Although both DnmA and FisA, are essential for mitochondrial fission, participate in peroxisomal division and are fully required for HO-induced mitochondrial division, they also appear to play differential functions. Despite their lack of mitochondrial division, and mutants segregate mitochondria to conidiogenic cells and produce viable conidia that inherit a single mitochondrion. During sexual differentiation, and mutants develop fruiting bodies (cleistothecia) that differentiate excessive ascogenous tissue and a reduced number of viable ascospores. and mutants show decreased respiration and notably high levels of mitochondrial reactive oxygen species (ROS), which likely correspond to superoxide. Regardless of this, mutants can respond to an external HO challenge by re-localizing the MAP kinase-activated protein kinase (MAPKAP) SrkA from the cytoplasm to the nuclei. Our results show that ROS levels regulate mitochondrial dynamics while a lack of mitochondrial fission results in lower respiration, increased mitochondrial ROS and developmental defects, indicating that ROS, mitochondrial division and development are critically interrelated processes.

摘要

发动蛋白样蛋白Drp1及其受体Fis-1是动物和酵母细胞中线粒体和过氧化物酶体分裂所必需的。在此,我们表明,在该真菌中,缺乏Drp1和Fis-1的同源物DnmA和FisA会导致严重的发育缺陷,导致菌丝生长以及无性和有性孢子形成显著减少,其中一些缺陷会因不同碳源而加剧或部分得到补救。尽管DnmA和FisA都是线粒体分裂所必需的,参与过氧化物酶体分裂并且是HO诱导的线粒体分裂所完全必需的,但它们似乎也发挥着不同的功能。尽管缺乏线粒体分裂, 突变体仍将线粒体分离到产孢细胞中,并产生可存活的分生孢子,这些分生孢子继承单个线粒体。在有性分化过程中, 突变体发育出子实体(闭囊壳),这些子实体分化出过多的产囊组织和数量减少的可存活子囊孢子。 突变体显示呼吸作用降低,线粒体活性氧(ROS)水平显著升高,这可能对应于超氧化物。尽管如此, 突变体可以通过将丝裂原活化蛋白激酶激活的蛋白激酶(MAPKAP)SrkA从细胞质重新定位到细胞核来应对外部HO挑战。我们的结果表明,ROS水平调节线粒体动力学,而线粒体分裂的缺乏会导致呼吸作用降低、线粒体ROS增加和发育缺陷,表明ROS、线粒体分裂和发育是密切相关的过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9e8/7232558/66c13c37ca16/fmicb-11-00837-g001.jpg

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