| First Author | Enkhmandakh B | Year | 2016 |
| Journal | Genesis | Volume | 54 |
| Issue | 7 | Pages | 407-12 |
| PubMed ID | 27194223 | Mgi Jnum | J:236328 |
| Mgi Id | MGI:5805740 | Doi | 10.1002/dvg.22948 |
| Citation | Enkhmandakh B, et al. (2016) Generation of a mouse model for a conditional inactivation of Gtf2i allele. Genesis 54(7):407-12 |
| abstractText | The multifunctional transcription factor TFII-I encoded by the Gtf2i gene is expressed at the two-cell stage, inner cell mass, trophectoderm, and early gastrula stages of the mouse embryo. In embryonic stem cells, TFII-I colocalizes with bivalent domains and depletion of Gtf2i causes embryonic lethality, neural tube closure, and craniofacial defects. To gain insight into the function of TFII-I during late embryonic and postnatal stages, we have generated a conditional Gtf2i null allele by flanking exon 3 with loxP sites. Crossing the floxed line with the Hprt-Cre transgenic mice resulted in inactivation of Gtf2i in one-cell embryo. The Cre-mediated deletion of exon 3 recapitulates a genetic null phenotype, indicating that the conditional Gtf2i line is a valuable tool for studying TFII-I function during embryonic development. genesis 54:407-412, 2016. (c) 2016 Wiley Periodicals, Inc. |
