4.7 Article

Loxl2 and Loxl3 Paralogues Play Redundant Roles during Mouse Development

期刊

出版社

MDPI
DOI: 10.3390/ijms23105730

关键词

lysyl oxidases; Loxl2; Loxl3; epistasis analysis; embryonic lethality

资金

  1. Spanish Ministry of Science and Innovation MCIN [SAF2016-76504-R, PID2019-111052RB-100]
  2. Spanish Institute of Health Carlos III [CIBERONC CCB16/12/00295]
  3. EU-FEDER funds
  4. Worldwide Cancer Research [16-0295]

向作者/读者索取更多资源

This study found that the lack of LOXL3 leads to perinatal lethality and abnormal skeletal development in mice, and LOXL2 and LOXL3 may have overlapping functions during mouse development. The widespread expression of LOXL2 can suppress the lethality associated with LOXL3 knockout mice.
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 Loxl2 and Loxl3 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.

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