Ncor1 (nuclear receptor co-repressor 1; N-CoR) is a regulator of erythrocyte, thymocyte and neural development processes. 

A 3 kb genomic sequence encoding the 5' SIN3 interaction domain (SID1) in Ncor1 is replaced with a neomycin resistance gene in this targeted knockout allele. Protein expression is not detectable in mouse embryonic fibroblasts (MEFs) derived from homozygotes. Homozygous embryos die between E13.5 and E15.5 and exhibit defects in developmental progression of specific erythrocyte, thymocyte, and neural events. Homozygotes demonstrate a red blood cell development deficiency, T cell development deficiency, and a neuronal deficiency. 

At E13.5, homozygous embryos are markedly pale, anemic, and on average 80% smaller than wildtype or heterozgyous littermates. Hematocrit levels are severely reduced. Peripheral blood smears from these mice show fewer non-nucleated erythroctyes, but many more nucleated erythroblasts than wildtype controls.

At E14.5, the thymus is markedly smaller in homozygous embryos. The total number of live thymocytes is reduced approximately 8-fold in cultured thymii, and an increased rate of cell death is observed. T cell development is arrested at the double-negative stage, with only 3% of thymocytes expressing both CD4 and CD8.

The relative size of the developing thalamus is reduced in homozygous embryos by E12.5, becoming increasingly more pronounced by E15. Nissl-staining of coronal brain sections reveals that specific thalamic nuclei, such as the lateral geniculate nucleus, are markedly smaller in homozygous embryos. No evidence of apoptosis is detected. Data suggests that this gene is a principal regulator of neural stem cells, and controls differentiation of neural stem cells into astrocytes.

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The 5' SIN3 interaction domain (SID1) of Ncor1 is replaced with a neomycin resistance gene in this targeted knockout allele. Homozygous embryos die between E13.5 and E15.5 and exhibit defects in developmental progression of specific erythrocyte, thymocyte, and neural events.

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