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Generating a Heat-Tolerance Mouse Model.

Jun Liu1, Paul J Verma2

  • 1Stem Cells and Genome Editing, Genomics and Cellular Sciences, Agriculture Victoria Research, Bundoora, VIC, Australia. jun.liu@agriculture.vic.gov.au.

Methods in Molecular Biology (Clifton, N.J.)
|June 13, 2022
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Summary
This summary is machine-generated.

Researchers created a mouse model with a prolactin receptor (PRLR) gene mutation identical to that found in slick cattle. This new model can help study thermoregulation and heat tolerance mechanisms.

Keywords:
CRISPRGenome editingHeat-toleranceHomology-directed repairProlactin receptorThermoregulationZygote microinjection

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Area of Science:

  • Genetics
  • Animal Models
  • Physiology

Background:

  • Mouse models are crucial for understanding genetic diseases and livestock traits.
  • A prolactin receptor (PRLR) mutation causes hair morphology changes in slick cattle, impacting more than just lactation.
  • Understanding these mutations aids fundamental and applied research.

Purpose of the Study:

  • To generate a knock-in mouse model with the specific prolactin receptor (PRLR) gene mutation found in slick cattle.
  • To establish a valuable animal model for investigating thermoregulation and heat tolerance.

Main Methods:

  • Utilized Cas9-mediated genome editing.
  • Employed homology-directed repair (HDR) in mouse zygotes.
  • Targeted the specific locus of the prolactin receptor (PRLR) gene.

Main Results:

  • Successfully generated a knock-in mouse model carrying the identical PRLR mutation observed in slick cattle.
  • The created mouse model accurately replicates the genetic basis of the slick cattle phenotype.

Conclusions:

  • The novel mouse model provides a platform for studying the PRLR gene's role in thermoregulation.
  • This research facilitates deeper understanding of heat tolerance mechanisms in livestock through a relevant animal model.