Open AccessReduced Sperm Count and Normal Fertility in Male Mice with Targeted Disruption of the ADP-Ribosylation Factor-Like 4 (Arl4) Gene
Author(s) -
Annette Schürmann,
S Koling,
Stephan Jacobs,
Paul Säftig,
Sharon Wald Krauss,
Gunther Wennemuth,
Reinhart Kluge,
HansGeorg Joost
Publication year - 2002
Publication title -
molecular and cellular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.14
H-Index - 327
eISSN - 1067-8824
pISSN - 0270-7306
DOI - 10.1128/mcb.22.8.2761-2768.2002
Subject(s) - biology , spermatogenesis , sperm , meiosis , andrology , gene , germ cell , adp ribosylation factor , spermatocyte , medicine , endocrinology , microbiology and biotechnology , genetics , cell , golgi apparatus
The ADP-ribosylation factor-like protein 4 (ARL4) is a 22-kDa GTP-binding protein which is abundant in testes of pubertal and adult rodents but absent in testes from prepubertal animals. During testis development, ARL4 expression starts at day 16 when the spermatogenesis proceeds to the late pachytene. In the adult testis, the ARL4 protein was detected in pre- and postmeiotic cells, spermatocytes, and spermatides, but not in spermatogonia and mature spermatozoa. MouseArl4 -null mutants generated by targeted disruption of theArl4 gene were viable and grew normally; male as well as femaleArl4−/− mice were fertile. However, inactivation of theArl4 gene resulted in a significant reduction of testis weight and sperm count by 30 and 60%, respectively, without reduction of litter size or frequency. It is suggested that the disruption ofArl4 produces a moderate retardation of germ cell development, possibly at the stage of meiosis.