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A heterozygous deficiency in protein phosphatase Ppm1b results in an altered ovulation number in mice
Naoki Ishii1, Takujiro Homma1, Ren Watanabe2
1Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University, Yamagata, Yamagata 990‑9585, Japan.
Abstract:
Ppm1b, a metal‑dependent serine/threonine protein phosphatase, catalyzes the dephosphorylation of a variety of phosphorylated proteins. Ppm1b‑/‑ mouse embryos die at the fertilized oocyte stage, whereas Ppm1b+/‑ mice with a C57BL/6 background exhibit no phenotypic abnormalities. Because the C57BL/6 strain produces a limited number of pups, in an attempt to produce Ppm1b‑/‑ mice, congenic Ppm1b+/‑ mice with an ICR background were established, which are more fertile and gave birth to more pups. As a result, however, no Ppm1b‑/‑ offspring were obtained when pairs of Ppm1b+/‑ ICR mice were bred again. Ppm1b+/‑ male and female ICR mice were analyzed from the viewpoint of fecundity. The Ppm1b haploinsufficiency had no effect on testicular weight or the number of sperm in male mice. Despite the fact that the levels of Ppm1b protein in the ovaries of sexually mature Ppm1b+/‑ mice were decreased compared with those of Ppm1b+/+ mice, there appeared to be no significant difference in the histological appearance of the ovaries, litter sizes or plasma progesterone levels at the estrous stage. When superovulation was induced by stimulation using a hormone treatment, the number of ovulated oocytes were the same for Ppm1b+/‑ and Ppm1b+/+ mice at 4 weeks of age when the estrous cycle did not proceed, however, the number of ovulated oocytes was lower in sexually mature Ppm1b+/‑ mice at 11 weeks of age compared with Ppm1b+/+ mice in the first and the second superovulation cycles. These collective results suggest that follicle development is excessive in Ppm1b+/‑ mice, and that this leads to a partial depletion of matured follicles and a corresponding decrease in the number of ovulated oocytes.
Insights
Protein phosphatase 1b (Ppm1b) haploinsufficiency in mice leads to ovarian follicle development issues. This results in fewer ovulated oocytes in mature Ppm1b+/- mice, impacting reproductive potential.
Area of Science:
- Molecular Biology
- Reproductive Biology
- Genetics
Background:
- Protein phosphatase 1b (Ppm1b) is a serine/threonine phosphatase crucial for dephosphorylating various proteins.
- Ppm1b knockout mouse embryos are not viable, dying at the fertilized oocyte stage.
- Heterozygous Ppm1b+/- mice on a C57BL/6 background show no abnormalities, but lower fertility rates in this strain prompted using an ICR background.
Purpose of the Study:
- To investigate the reproductive capacity and potential phenotypic abnormalities in Ppm1b haploinsufficient mice on an ICR background.
- To determine the effect of Ppm1b haploinsufficiency on male and female reproductive parameters, particularly oocyte ovulation.
Main Methods:
- Breeding of Ppm1b+/- ICR mice to assess offspring viability and reproductive success.
- Analysis of male reproductive parameters including testicular weight and sperm count.
- Assessment of female reproductive parameters: ovarian histology, litter size, progesterone levels, and superovulation response at different ages.
Main Results:
- No Ppm1b-/- offspring were obtained from Ppm1b+/- ICR mouse crosses.
- Male Ppm1b+/- mice showed no significant differences in testicular weight or sperm count.
- Mature female Ppm1b+/- mice exhibited reduced Ppm1b protein levels in ovaries but normal histology and litter sizes; however, they showed a decreased number of ovulated oocytes after superovulation induction compared to Ppm1b+/+ mice.
Conclusions:
- Ppm1b haploinsufficiency in mice does not affect male fertility.
- Excessive follicle development in Ppm1b+/- female mice leads to partial depletion of mature follicles.
- This depletion results in a decreased number of ovulated oocytes in sexually mature Ppm1b+/- mice, indicating a potential impact on female reproductive function.
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