TY - JOUR
AU1 - Sakurai, Nobuyuki
AU2 - Fujihara, Yoshitaka
AU3 - Kobayashi, Kiyonori
AU4 - Ikawa, Masahito
AB - INTRODUCTIONSpermatozoa acquire their ability to fertilize and capability of forward motility during epididymal transit. This event is called epididymal sperm maturation. The epididymis comprises a dense convoluted duct that measures just over 1 m in mice (see review by Hinton et al.1) and is divided into the caput, corpus, and cauda. Caput‐spermatozoa have very low fertilizing potential, although rates vary between species. However, most spermatozoa in the distal part of the epididymis can fertilize oocytes (see review by Bedford2), suggesting that some key factors controlling sperm maturation in the epididymis exist in the caput and/or corpus segment. Our laboratory has been searching genes predominantly expressed in the epididymis using a transcriptome database3 and generating knockout (KO) mice to investigate their physiological functions.4–6 In the present study, we focused on epididymis‐enriched lipocalin and Ly6 family genes.The lipocalin family consists of many small, diverse secreted proteins and is defined by a highly conserved three‐dimensional structure.7,8 Most lipocalin family genes are evolutionarily conserved in humans and mice, forming clusters on chromosome 2 in mice.9 LCN2 is secreted in the female reproductive tract and binds to spermatozoa. Although Lcn2 KO male mice are fully fertile, female mice show a significant reduction in pregnancy rate,10,11 suggesting 
TI - CRISPR/Cas9‐mediated disruption of lipocalins, Ly6g5b, and Ly6g5c causes male subfertility in mice
JF - Andrology
DO - 10.1111/andr.13350
DA - 2024-07-01
UR - https://www.deepdyve.com/lp/wiley/crispr-cas9-mediated-disruption-of-lipocalins-ly6g5b-and-ly6g5c-causes-mb3Gouy32F
SP - 981
EP - 990
VL - 12
IS - 5
DP - DeepDyve
ER -