Publication: Ovarian development in mice bearing homozygous or heterozygous null mutations in zona pellucida glycoprotein gene mZP3
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Date
1998
Authors
Wassarman, P.M. ; Liu, C. ; Chen, J. ; Qi, H. ; Litscher, E.S.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
The plasma membrane of all mammalian
eggs is surrounded by a thick extracellular coat, the zonu
pellirc.id(i (ZP), whose paramount function is to regulate
species-specific fertilization. The mouse egg ZP is
composed of only three glycoproteins, mZPI -3, that are
synthesized and secreted exclusively by oocytes during
their 2-3 week growth phase. Disruption of the rnZP3
gene by targeted mutagenesis in embryonic stem
(ES) cells yields mice heterozygous ( r n ~ P 3 + / -o)r
hornozygous ( r n ~ P 3 - / -f)o r the null mutation. As
expected, male mice bearing the null mutation are
indistinguishable from wild-type males with respect to
viability and fertility. Female m ~ ~ 3 +m/ic-e are as fertile
as wild-type animals, but their eggs have a thin ZP (-2.7
pm thick) as compared to the ZP (-6.2 pm thick) of eggs
from wild-type animals. On the other hand, female
rn~P3-/m- ice are infertile and their eggs lack a ZP. The
infertility apparently is due to the lack of a sufficient
number of eggs in oviducts of superovulated ~ZPJ-lfemales.
Light micrographs reveal that development of
ovarian follicles is often retarded in rnz~3- l -m ice as
compared to wild-type animals. This is manifested as
reduced ovarian weights, reduced numbers of Graafian follicles, and reduced numbers of fully-grown oocytes in
I ~ Z P ~ -f/em- ales. I t seems likely that the pleiotropic
effects of the homozygous null mutation on ovarian
development may be due, at least in part, to disruption of
intercellular communication between growing oocytes
and their surrounding follicle cells.
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