TY - JOUR
T1 - Rare mutations in the complement regulatory gene CSMD1 are associated with male and female infertility
AU - Lee, Arthur S.
AU - Rusch, Jannette
AU - Lima, Ana C.
AU - Usmani, Abul
AU - Huang, Ni
AU - Lepamets, Maarja
AU - Vigh-Conrad, Katinka A.
AU - Worthington, Ronald E.
AU - Mägi, Reedik
AU - Wu, Xiaobo
AU - Aston, Kenneth I.
AU - Atkinson, John P.
AU - Carrell, Douglas T.
AU - Hess, Rex A.
AU - O’Bryan, Moira K.
AU - Conrad, Donald F.
N1 - Publisher Copyright:
© 2019, The Author(s).
PY - 2019/12/1
Y1 - 2019/12/1
N2 - Infertility in men and women is a complex genetic trait with shared biological bases between the sexes. Here, we perform a series of rare variant analyses across 73,185 women and men to identify genes that contribute to primary gonadal dysfunction. We report CSMD1, a complement regulatory protein on chromosome 8p23, as a strong candidate locus in both sexes. We show that CSMD1 is enriched at the germ-cell/somatic-cell interface in both male and female gonads. Csmd1-knockout males show increased rates of infertility with significantly increased complement C3 protein deposition in the testes, accompanied by severe histological degeneration. Knockout females show significant reduction in ovarian quality and breeding success, as well as mammary branching impairment. Double knockout of Csmd1 and C3 causes non-additive reduction in breeding success, suggesting that CSMD1 and the complement pathway play an important role in the normal postnatal development of the gonads in both sexes.
AB - Infertility in men and women is a complex genetic trait with shared biological bases between the sexes. Here, we perform a series of rare variant analyses across 73,185 women and men to identify genes that contribute to primary gonadal dysfunction. We report CSMD1, a complement regulatory protein on chromosome 8p23, as a strong candidate locus in both sexes. We show that CSMD1 is enriched at the germ-cell/somatic-cell interface in both male and female gonads. Csmd1-knockout males show increased rates of infertility with significantly increased complement C3 protein deposition in the testes, accompanied by severe histological degeneration. Knockout females show significant reduction in ovarian quality and breeding success, as well as mammary branching impairment. Double knockout of Csmd1 and C3 causes non-additive reduction in breeding success, suggesting that CSMD1 and the complement pathway play an important role in the normal postnatal development of the gonads in both sexes.
UR - http://www.scopus.com/inward/record.url?scp=85073176208&partnerID=8YFLogxK
U2 - 10.1038/s41467-019-12522-w
DO - 10.1038/s41467-019-12522-w
M3 - Article
C2 - 31604923
AN - SCOPUS:85073176208
SN - 2041-1723
VL - 10
JO - Nature communications
JF - Nature communications
IS - 1
M1 - 4626
ER -