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Inactivation of the Rps4 gene on the mouse X chromosome

A R Zinn1, S L Bressler, P Beer-Romero

  • 1Howard Hughes Research Laboratories, Whitehead Institute, Cambridge, Massachusetts.

Genomics
|December 1, 1991
PubMed

Insights

Mouse Rps4 is subject to X inactivation, unlike human RPS4X. This difference in X inactivation may explain why X monosomy is less severe in mice than in humans, impacting Turner syndrome research.

Area of Science:

  • Genetics
  • Developmental Biology
  • Molecular Biology

Background:

  • The human RPS4X and RPS4Y genes encode ribosomal protein S4 isoforms.
  • Haploinsufficiency of these genes is implicated in Turner syndrome.
  • Human RPS4X escapes X inactivation despite its proximity to the X-inactivation center.

Purpose of the Study:

  • To investigate the X inactivation status of the mouse Rps4 gene, the homolog of human RPS4X.
  • To compare the X inactivation behavior of mouse Rps4 with human RPS4X.
  • To understand the genetic basis for differential severity of X monosomy phenotypes between mice and humans.

Main Methods:

  • Cloned the mouse Rps4 gene.
  • Utilized allelic variation in Rps4 for experimental tracking.
  • Examined Rps4 gene transcription from active and inactive X chromosomes in vivo using female mice with an X-autosome translocation.

Main Results:

  • Mouse Rps4 is subject to X inactivation.
  • Human RPS4X escapes X inactivation.
  • Demonstrated differential regulation of homologous genes between species.

Conclusions:

  • Mouse Rps4 undergoes X inactivation, contrasting with human RPS4X.
  • This difference in X inactivation may contribute to the milder phenotype of X monosomy in mice compared to humans.
  • Provides insights into species-specific gene regulation and its impact on developmental disorders.

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