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Related Concept Videos

Lethal Alleles02:41

Lethal Alleles

Agouti: A Lethal Allele
Lucien Cuénot discovered lethal alleles in 1905 while studying the inheritance of coat color in mice. The agouti gene is responsible for the color of the coat in mice. This gene codes for an agouti-signaling protein, which is responsible for melanin distribution in mammals. The wild-type allele gives rise to gray-brown coat color in mice, while the mutant allele gives rise to yellow coat color. In addition to coat color, the agouti gene is associated with the yellow...
Meiosis II02:02

Meiosis II

Meiosis II entails cell division and segregation of the sister chromatids, resulting in the production of four unique haploid gametes. The steps for meiosis II are similar to mitosis, except that meiosis II occurs in haploid cells, whereas mitosis occurs in diploid cells.
The timing and cell division patterns of meiosis differ between males and females. In male meiosis, the centrosomes are part of the formation of the meiotic spindle. However, in oocytes, including that of humans, Drosophila,...

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Related Experiment Video

Updated: Jun 24, 2026

Assessment of Perigenital Sensitivity and Prostatic Mast Cell Activation in a Mouse Model of Neonatal Maternal Separation
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Mmp2 Deficiency Leads to Defective Parturition and High Dystocia Rates in Mice.

Rotem Kalev-Altman1,2, Gal Becker2, Tamar Levy1

  • 1The Koret School of Veterinary Medicine, The RH Smith Faculty of Agriculture, Food and Environment, The Hebrew University of Jerusalem, Rehovot 7610001, Israel.

International Journal of Molecular Sciences
|December 9, 2023
PubMed
Summary

Loss of matrix metalloproteinase-2 (MMP2) causes significant dystocia in mice due to uterine fibrosis. This study reveals MMP2

Keywords:
MMP2MMP9double knockoutdystociafibrosisgelatinasematrix metalloproteinasemyometriumuterine

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Area of Science:

  • Reproductive biology
  • Molecular and cell biology
  • Biochemistry

Background:

  • Parturition involves complex uterine changes, including extracellular matrix (ECM) remodeling, essential for mammalian reproduction.
  • Matrix metalloproteinases (MMPs), specifically MMP2 and MMP9, are implicated in uterine ECM remodeling during pregnancy and parturition.
  • The functional consequences of MMP2 and MMP9 deficiency on parturition remain largely unexplored.

Purpose of the Study:

  • To investigate the in vivo effects of Mmp2 and/or Mmp9 gene elimination on parturition.
  • To determine the role of MMP2 and MMP9 in uterine structural integrity and remodeling during the parturition process.

Main Methods:

  • Generation and analysis of single (Mmp2-/- or Mmp9-/-) and double (Mmp2-/- Mmp9-/-) knockout mice.
  • Assessment of dystocia rates in different genotypes.
  • Histological examination of uterine and cervical tissues from nulliparous mice at various ages.

Main Results:

  • Mmp2-/- and double knockout (dKO) mice exhibited high dystocia rates (40-55%), unlike Mmp9-/- and wild-type mice.
  • Histological analysis of Mmp2-/- uteri revealed significant structural alterations, including enlarged myometrial and endometrial layers and luminal cavity.
  • Evidence of increased collagen deposition and fibrosis in the Mmp2-/- myometrium was observed.

Conclusions:

  • MMP2 plays a critical role in myometrium remodeling essential for successful mammalian parturition.
  • Loss of MMP2 activity leads to uterine fibrosis and structural abnormalities, resulting in dystocia.
  • This study identifies a novel cause of parturition failure linked to MMP2 deficiency in uterine tissue.