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Simhadri, S. et al. Male fertility defect associated with disrupted BRCA1-PALB2 interaction in mice.
Both male and female homozygous mutant (Sulf1−/−) mice were capable of generating offspring, indicating no obvious fertility defect (data not shown).
This is consistent with our previous observations indicating the forced expression of normal Roc1a from the Roc1b promoter can partially rescue the Roc1b male fertility defect [25].
The C. elegans infection assay was carried out as described by Kurz et al. [25] except that the Fer-15 mutant line, which has a temperature sensitive fertility defect, were used rather than wild type N2 worms.
At all three temperatures tested 15°C, 20°C and 25°C the brood size of the pk924 worms was about 50% that of the wild-type worms (Fig. 2A C and Table 1), suggesting a non-temperature sensitive fertility defect upon loss of Ce HCF-1 function.
The most likely explanation was a fertility defect.
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We focused on M601, which displayed clear fertility defects as homozygotes, while M602 were fertile and M603 were lethal.
Sex-specific fertility defects can be determined by in vitro cross-fertilization studies, where mutant gametes are cross-fertilized with gametes of parasite lines that produce either only fertile male or female gametes (Mair et al., 2010; van Dijk et al., 2010).
Most interestingly, the female fertility defects are dramatically enhanced when one copy of the dcr-1 gene is missing and Dicer-1 protein co-immunoprecipitates with R2D2 antisera.
Telomere dysfunction results in fertility defects in a number of organisms.
The combination of primordial germ cell deficit and spermatogonial depletion contributes to severe fertility defects in Pin1-null mice.
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