Deletion of Kallikrein-related peptidases ( Klks ) has no effect on fertility in mice

TL;DR

Deleting four kallikrein-related peptidase genes in mice did not affect fertility or health, suggesting these genes are not essential for reproduction.

Contribution

Generated a mouse model with deletions of four Klk genes and demonstrated their non-essential role in fertility.

Findings

Male and female knockout mice were fertile with no health defects.

The Klk1b3, Klk1b4, Klk1b5, and Klk1 genes are not required for reproductive function in mice.

Abstract

Kallikreins (KLKs) are serine peptidases. It was established that
Klks
are estrogen-target genes in mouse uteri. However, the functional requirement of KLK family in the uterine function during reproduction is unknown. Here we generated a compound deletion of
Klk1b3, Klk1b4, Klk1b5,
and
Klk1
in a mouse model using CRISPR/Cas9 strategy with four single guide RNAs (sgRNAs) to target the second exon of these four genes that are aligned back-to-back in a single locus spanning 32.95 kb on chromosome 7. We found that both male and female knockout mice are fertile with no apparent health defect compared to wild-type controls. Our data suggest that
Klk1b3, Klk1b4, Klk1b5,
and
Klk1
are not necessary for male and female reproductive function in mice.

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