| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-110 |
DRI_Outcome |
denotes |
Gender of the embryo contributes to CAG instability in transgenic mice containing a Huntington's disease gene. |
| T2 |
111-199 |
DRI_Background |
denotes |
Gender is known to influence the transmission of trinucleotide repeats in human disease. |
| T3 |
200-321 |
DRI_Approach |
denotes |
However, the molecular basis for the parent-of-origin effect associated with trinucleotide repeat expansion is not known. |
| T4 |
322-491 |
DRI_Approach |
denotes |
We have followed, during transmission, the fate of the CAG trinucleotide repeat in a transgene containing the exon 1 portion of the human Huntington's disease (HD) gene. |
| T5 |
492-583 |
DRI_Background |
denotes |
Similar to humans, the mouse transmits expansions predominantly through the male germ line. |
| T6 |
584-722 |
DRI_Outcome |
denotes |
Surprisingly, we find that the CAG repeat size of the mutant human HD gene is different in male and female progeny from identical fathers. |
| T7 |
723-811 |
DRI_Approach |
denotes |
Males predominantly expand the repeat whereas females predominantly contract the repeat. |
| T8 |
812-921 |
DRI_Approach |
denotes |
In contrast to the classic definition of imprinting, CAG expansion is influenced by the gender of the embryo. |
| T9 |
922-1053 |
DRI_Outcome |
denotes |
Our results raise the possibility that there are X- or Y-encoded factors that influence repair or replication of DNA in the embryo. |
| T10 |
1054-1189 |
DRI_Background |
denotes |
Gender dependence in the embryo may explain why expansion in HD from premutation to disease primarily occurs through the paternal line. |
