Stanfel M N, Moses K A, Carson J A, Zimmer D B, DeMayo F, Schwartz R J, Zimmer W E
Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas, USA.
Genesis. 2006 Nov;44(11):550-5. doi: 10.1002/dvg.20250.
The genetic locus of Nkx3.1, an early murine marker of sclerotome and prostate development, was disrupted by a knock in of CRE recombinase via homologous recombination in embryonic stem cells. Cell fate mapping revealed previously unidentified cell lineages expanded from Nkx3.1-expressing cell populations and recapitulated reported Nkx3.1 expression patterns. In lineage trace experiments of E18.5 Nkx3.1-CRE; R26R embryos novel staining was observed in areas of the lungs, portions of the duodenum, and vertebral elements of the skeleton. beta-galactosidase activity measured in Nkx3.1-CRE; R26R and Nkx3.2-CRE; R26R embryos was observed in overlapping regions of the sclerotome but no apparent change in Nkx3.1 expression was seen in the Nkx3.2 mutants by in situ hybridization.
Nkx3.1是硬骨节和前列腺发育的早期小鼠标志物，其基因座通过在胚胎干细胞中进行同源重组敲入CRE重组酶而被破坏。细胞命运图谱揭示了从表达Nkx3.1的细胞群体扩展而来的先前未被识别的细胞谱系，并重现了已报道的Nkx3.1表达模式。在E18.5 Nkx3.1-CRE; R26R胚胎的谱系追踪实验中，在肺区域、十二指肠部分和骨骼的椎骨元件中观察到了新的染色。在Nkx3.1-CRE; R26R和Nkx3.2-CRE; R26R胚胎中测量的β-半乳糖苷酶活性在硬骨节的重叠区域中观察到，但通过原位杂交在Nkx3.2突变体中未观察到Nkx3.1表达有明显变化。
