The Drosophila dec-1 gene encodes multiple proteins that are required for female fertility and proper eggshell morphogenesis. Genetic and immunolocalization data suggest that the different DEC-1 proteins are functionally distinct. To identify regions within the proteins with potential biological significance, we cloned and sequenced the D. yakuba and D. virilis dec-1 homologs. Interspecies comparisons of the predicted translation products revealed rapidly evolving sequences punctuated by blocks of conserved amino acids. Despite extensive amino acid variability, the proteins produced by the different dec-1 homologs were functionally interchangeable. The introduction of transgenes containing either the D. yakuba or the D. virilis dec-1 open reading frames into a D. melanogaster DEC-1 protein null mutant was sufficient to restore female fertility and wild-type eggshell morphology. Normal expression and extracellular processing of the DEC-1 proteins was correlated with the phenotypic rescue. The nature of the conserved features highlighted by the evolutionary comparison and the molecular resemblance of some of these features to those found in other extracellular proteins suggests functional correlates for some of the multiple DEC-1 derivatives.
Plant death is the most common effect resulting from the application of glyphosate, the active ingredient in the herbicide Roundup®. Individual seedlings of the morning glory, Ipomoea purpurea L. Roth, however, have been shown to exhibit tolerance to glyphosate, surviving after what should have been a lethal dose. Those that grow and reach reproductive maturity often exhibit deformed anthers within what appear to be normally developed flowers. Ipomoea purpurea has a mixed mating system and normally has hermaphroditic flowers that are capable of both selfing and outcrossing. The deformed anthers do not produce pollen, essentially converting a hermaphroditic flower to a female. Here we describe this morphological change and investigate the reproductive consequences of anther deformation. First, there is phenotypic variation for the propensity of an individual to exhibit male sterility through deformed anthers in response to treatment, but a series of field and greenhouse studies suggest that this variation is not genetic. The male sterility is also transient; within an individual, the frequency of flowers with deformed anthers declines over time. Although flowers with deformed anthers do not produce pollen, we observed mixed effects on female function of such flowers. In the greenhouse, flowers with deformed anthers that were hand-pollinated produced as many seeds as flowers with normal anthers, suggesting no effect on female fertility. In the field, however, plants with a higher proportion of anther deformation set significantly fewer seeds than those untreated, suggesting either reduced female fertility, or a reproductive penalty in flowers with deformed anthers due to the inability to self pollinate. Thus, the presence of this trait could alter the selfing to outcrossing ratio in populations that are sprayed with the herbicide. Individuals that exhibited a higher proportion of anther deformation also produce fewer total flowers than untreated plants, suggesting that anther deformation is part of a suite of responses to damage by glyphosate.
Androgens synergise with FSH in female reproduction but the nature of their interaction in ovarian function and fertility is not clear. In the present study, we investigated this interaction, notably whether higher endogenous FSH can overcome defective androgen actions in androgen receptor (AR)-knockout (ARKO) mice. We generated and investigated the reproductive function of mutant mice exhibiting AR resistance with or without expression of human transgenic FSH (Tg-FSH). On the background of inactivated AR signalling, which alone resulted in irregular oestrous cycles and reduced pups per litter, ovulation rates and antral follicle health, Tg-FSH expression restored follicle health, ovulation rates and litter size to wild-type levels. However, Tg-FSH was only able to partially rectify the abnormal oestrous cycles observed in ARKO females. Hence, elevated endogenous FSH rescued the intraovarian defects, and partially rescued the extraovarian defects due to androgen insensitivity. In addition, the observed increase in litter size in Tg-FSH females was not observed in the presence of AR signalling inactivation. In summary, the findings of the present study reveal that FSH can rescue impaired female fertility and ovarian function due to androgen insensitivity in female ARKO mice by maintaining follicle health and ovulation rates, and thereby optimal female fertility.