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Loxl2 和 Loxl3 基因在小鼠发育过程中发挥冗余作用。

Loxl2 and Loxl3 Paralogues Play Redundant Roles during Mouse Development.

机构信息

Departamento de Bioquímica, Instituto de Investigaciones Biomédicas Alberto Sols, Universidad Autónoma de Madrid, CSIC-UAM, 28029 Madrid, Spain.

Instituto de Investigación Sanitaria del Hospital Universitario La Paz-IdiPAZ, 28029 Madrid, Spain.

出版信息

Int J Mol Sci. 2022 May 20;23(10):5730. doi: 10.3390/ijms23105730.

DOI:10.3390/ijms23105730
PMID:35628534
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9144032/
Abstract

Lysyl oxidase-like 2 (LOXL2) and 3 (LOXL3) are members of the lysyl oxidase family of enzymes involved in the maturation of the extracellular matrix. Both enzymes share a highly conserved catalytic domain, but it is unclear whether they perform redundant functions in vivo. In this study, we show that mice lacking Loxl3 exhibit perinatal lethality and abnormal skeletal development. Additionally, analysis of the genotype of embryos carrying double knockout of and genes suggests that both enzymes have overlapping functions during mouse development. Furthermore, we also show that ubiquitous expression of Loxl2 suppresses the lethality associated with Loxl3 knockout mice.

摘要

赖氨酰氧化酶样蛋白 2(LOXL2)和 3(LOXL3)是赖氨酰氧化酶家族的成员,参与细胞外基质的成熟。两种酶都具有高度保守的催化结构域,但尚不清楚它们在体内是否具有冗余功能。在这项研究中,我们表明缺乏 Loxl3 的小鼠表现出围产期致死和骨骼发育异常。此外,对携带 和 基因双敲除胚胎基因型的分析表明,这两种酶在小鼠发育过程中具有重叠的功能。此外,我们还表明,LOXL2 的广泛表达可以抑制与 Loxl3 敲除小鼠相关的致死性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41ab/9144032/05098f75098b/ijms-23-05730-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41ab/9144032/ad0aff340c3e/ijms-23-05730-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41ab/9144032/46b1c0ac942e/ijms-23-05730-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41ab/9144032/05098f75098b/ijms-23-05730-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41ab/9144032/ad0aff340c3e/ijms-23-05730-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41ab/9144032/46b1c0ac942e/ijms-23-05730-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41ab/9144032/05098f75098b/ijms-23-05730-g003.jpg

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Targeted Deletion of Loxl3 by Col2a1-Cre Leads to Progressive Hearing Loss.通过Col2a1-Cre靶向缺失Loxl3导致进行性听力损失。
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