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Knock-Out and Wild-Type Mice1
Departments of Animal Sciences (C.S.R., D.B.L.), Veterinary Biomedical Sciences (V.K.G.), Biochemistry and Child Health (J.A.T., X.-H.Y., D.B.L.), University of Missouri, Columbia, Missouri 65211; Affinity BioReagents (J.S.), Golden, Colorado 80401; and The Population Council (M.P.H.), New York, New York 10021
Address all correspondence and requests for reprints to: Dr. Dennis B. Lubahn, University of Missouri, 163 ASRC East Campus Drive, Columbia, Missouri 65211. E-mail: asld{at}muccmail.missouri.edu
Estrogen receptor-
(ER) has been identified in the male
reproductive tract, but the role of estrogen in the male has not been
well characterized. In vivo mutations in ER genes
have demonstrated the necessity for ER-mediated action in male
fertility. We asked whether both ERß messenger RNA and protein were
present in the male reproductive tract of wild-type and ER knock-out
(ER KO) mice, and whether ERß could compensate for the lack of
ER in infertile male ER KO mice. Immunohistochemical localization
with both N- and C-terminal anti-ERß antibodies demonstrated that
ERß is present in the Leydig cells of the testes and in the
epithelium of both the efferent ductules and the initial segment of the
epididymis. RT-PCR amplification was used to confirm ERß
transcription in these tissues. In conclusion, we observed that ERß
messenger RNA and protein continue to be expressed in the Leydig cells,
elongated spermatids, efferent ductules, and the initial segment of the
epididymides of ER KO mice, but the presence of ERß is
not able to compensate for the absence of ER in male reproductive
function.
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