While inheritance of mutated alleles of highly penetrant tumor suppressor genes such as retinoblastoma or p53 predisposes individuals to a greatly increased risk of developing cancer, epidemiological data indicate that the majority of sporadic tumors in humans result from interactions of environment
Matrix metalloproteinase-9 maps to the distal end of chromosome 2 in the mouse
✍ Scribed by Leco, Kevin J. ;Harvey, Mark B. ;Hogan, Aileen ;Copeland, Neal G. ;Gilbert, Debra J. ;Jenkins, Nancy A. ;Edwards, Dylan R. ;Schultz, Gilbert A.
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 88 KB
- Volume
- 21
- Category
- Article
- ISSN
- 0192-253X
No coin nor oath required. For personal study only.
✦ Synopsis
The activity and expression of matrix metalloproteinase-9/gelatinase B (MMP-9), an enzyme implicated in the implantation process in mice, was investigated in normal and parthenogenetic blastocyst outgrowths. Conditioned media from parthenogenetic blastocysts after 4 days of culture had reduced levels of MMP-9 activity compared to conditioned medium from normal outgrowths. Levels of MMP-9 mRNA assayed by reverse transcription-polymerase chain reaction methods were also reduced in parthenogenetic blastocysts compared to normal outgrowths. Genetic mapping studies showed that Mmp9 maps to the distal end of chromosome 2 near the proximal boundary of a region affected by genomic imprinting. Both parental alleles of Mmp9, however, are expressed in 11.5-day embryos derived from interspecific crosses of Mus musculus and Mus spretus. Thus, loss of MMP-9 activity in parthenogenetic blastocysts does not appear to be due to imprinting but, rather, due to a defect of trophoblast giant cell proliferation and differentiation.
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