| First Author | Kratzer PG | Year | 1983 |
| Journal | Genetics | Volume | 104 |
| Issue | 4 | Pages | 685-98 |
| PubMed ID | 6618165 | Mgi Jnum | J:296660 |
| Mgi Id | MGI:6471729 | Doi | 10.1093/genetics/104.4.685 |
| Citation | Kratzer PG (1983) Expression of maternally and embryonically derived hypoxanthine phosphoribosyl transferase (HPRT) activity in mouse eggs and early embryos. Genetics 104(4):685-98 |
| abstractText | X-chromosome activity in early mouse development has been studied by a gene dosage method that involves measuring the activity level of the X-linked enzyme hypoxanthine phosphoribosyl transferase (HPRT) in single eggs and embryos from XO females and from females heterozygous for In(X)1H, a paracentric inversion of the X chromosome. The HPRT activity in oocytes increased threefold over a 24-hr period beginning after ovulation. Afterward, the activity plateaued in unfertilized eggs but continued to increase for at least 66 hr in presumed OY embryos. Both before and after ovulation, the level of activity in unfertilized eggs from In(X)/X females was twice that from XO females, and the distributions of activity in eggs for both sets of females remained unimodal. Beginning with the two-cell stage, distributions of activity for embryos from In(X)/X females were trimodal, which is evidence for embryonic activity. It is proposed that activation of a maternal mRNA or proenzyme is responsible for the HPRT activity increase in oocytes and early embryos and is supplemented by dosage-dependent activity of the embryonic Hprt gene as early as the two-cell stage. |
