Downregulation of the miR-143/145 cluster (also called Mirc32, microRNA cluster 32, including Mir143 and Mir145a) has been reported in colon cancer and other epithelial tumors. Overexpression of these miRNAs inhibits tumorigenesis, suggesting they function as cell-autonomous epithelial tumor suppressors. Mirc32 sequences are deleted in this miR-143/145Null/+ null targeted mutant strain. MiR-143/145 microRNA is undetectable in homozygous null mice. Germline deletion of these miRNAs results in no overt developmental defects and the targeted allele is transmitted at expected Mendelian ratios. Animals lacking Mirc32 show normal intestinal development, but epithelial regeneration after injury is dramatically impaired.Update February, 2019: Although the donating investigator reports no viability or fertility issues, colonies maintained at The Jackson Laboratory demonstrate that homozygotes are generally nonproductive. The few litters produced by homozygotes are very small, with pups often not surviving to weaning age. Heterozygote x heterozygote crosses also produce small litters (~ 5 pups).

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Mirc32 (associated with colon cancer and other epithelial tumors) is deleted in this miR-143/145Null/+ targeted mutant strain.

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