Matrix metalloproteinase-9 maps to the distal end of chromosome 2 in the mouse

被引:0
作者
Leco, KJ
Harvey, MB
Hogan, A
Copeland, NG
Gilbert, DJ
Jenkins, NA
Edwards, DR
Schultz, GA
机构
[1] UNIV CALGARY, DEPT MED BIOCHEM, CALGARY, AB T2N 4N1, CANADA
[2] PRINCESS MARGARET HOSP, ONTARIO CANC INST, TORONTO, ON M4X 1K9, CANADA
[3] QUEENSLAND UNIV TECHNOL, SCH LIFE SCI, BRISBANE, QLD, AUSTRALIA
[4] NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, MAMMALIAN GENET LAB, FREDERICK, MD 21701 USA
来源
DEVELOPMENTAL GENETICS | 1997年 / 21卷 / 01期
关键词
parthenogenetic embryos; trophoblast; imprinting;
D O I
10.1002/(SICI)1520-6408(1997)21:1<55::AID-DVG6>3.0.CO;2-7
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
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 io normal outgrowths. Geneiic mapping studies showed that Mmp9 maps to the distal end of chromosome 2 near the proxima 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 io a defect of trophoblast giant cell proliferation and differentiation. (C) 1997 Wiley-iiss, Inc.
引用
收藏
页码:55 / 60
页数:6
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