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某生物的选择性自噬基因中的一个无效等位基因 。 (注:原文“A null allele in the selective autophagy gene of .”表述不完整,缺少具体所指生物,这里只能按字面意思尽量准确翻译。)

A null allele in the selective autophagy gene of .

作者信息

Buddell Tyler, Quinn Christopher

机构信息

University of Wisconsin-Milwaukee, Milwaukee, WI, USA.

出版信息

MicroPubl Biol. 2022 Jul 20;2022. doi: 10.17912/micropub.biology.000598. eCollection 2022.

Abstract

The WDFY-3 protein is important for cargo selection during selective autophagy and for regulating axon termination. The C-terminal region of WDFY-3 contains BEACH, WD repeats, and FYVE-like domains, all of which are required for selective autophagy. WDFY-3 also contains a large N-terminal region that is relatively uncharacterized. Currently, is the only mutant allele that has been characterized for this gene. This allele features a small deletion that is predicted to disrupt the C-terminal region of the protein. Here, we used CRISPR Cas9 to produce a new allele that is a near complete deletion of the coding region. We report that, unlike the existing allele, this new null allele causes a weak overextension phenotype in the PLM axon. Like the existing allele, the new null allele can suppress PLM axon termination defects caused by an null allele. Creating and characterizing new alleles will increase our understanding of this gene and could help elucidate more of the gene's conserved functions.

摘要

WDFY-3蛋白在选择性自噬过程中的货物选择以及轴突终末调控方面具有重要作用。WDFY-3的C末端区域包含BEACH结构域、WD重复序列和类FYVE结构域,这些对于选择性自噬都是必需的。WDFY-3还包含一个相对未被充分研究的大的N末端区域。目前, 是该基因唯一已被鉴定的突变等位基因。这个等位基因有一个小的缺失,预计会破坏蛋白质的C末端区域。在此,我们使用CRISPR Cas9产生了一个新的 等位基因,它几乎完全缺失了编码区域。我们报告称,与现有的 等位基因不同,这个新的 无效等位基因在PLM轴突中导致了一种较弱的过度延伸表型。与现有的 等位基因一样,新的 无效等位基因可以抑制由 无效等位基因引起的PLM轴突终末缺陷。创建和鉴定新的 等位基因将增进我们对该基因的理解,并有助于阐明该基因更多的保守功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a47/9315409/55662ea44c9a/25789430-2022-micropub.biology.000598.jpg

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