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Effects of genetic background on cardiovascular and placental anomalies in the Ts16 mouse
Author(s) -
Villar Angela Jane,
Gillespie Anne Marie,
Ursell Philip C,
Epstein Charles J
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a446-c
Subject(s) - fetus , biology , trisomy , aneuploidy , andrology , embryo , aortic arch , genetics , chromosome , gene , microbiology and biotechnology , pathology , pregnancy , medicine , aorta
To investigate the genetic contribution to phenotypic variability in aneuploidy, we generated mice with trisomy 16 (Ts16) by mating [Rb(6.16)24Lub x Rb(16.17)7Bnr]F1 males with females from four inbred strains, BALB/cJ, C3H/HeJ,C57BL/6J, and DBA/2J. Among the four Ts16 strains generated, there were no significant differences in survival,weight,or length relative to euploid controls at either embryonic day (E) 14.5 or E17.5. All Ts16 fetuses exhibited gross morphological abnormalities that were not strain‐specific in occurrence or frequency. There was gross disorganization of the placenta with an increased area of spongiotrophoblast invading the labyrinth and a range of limited trophoblast cell invasion in all Ts16 fetuses relative to euploid controls. Interestingly, at E10.5, we observed pharyngeal arch artery (PAA) anomalies exclusively on the C3H/HeJ background. In contrast, at E17.5, in addition to ventricular and atrioventricular septal defects, a high frequency of aortic arch defects were detected in all Ts16 fetuses, regardless of genetic background. Taken together, the cardiovascular findings indicate that in the presence of three copies of murine chromosome 16 the development of PAA defects is strongly influenced by genetic background while the development of aortic arch anomalies in the absence of preexisting PAA anomalies, is not. These results provide the foundation for studying genomic‐based pathological conditions in the Ts16 murine model by analyzing strain‐specific differences in gene expression.