244 research outputs found

    A novel function for the presenilin family member spe-4: inhibition of spermatid activation in Caenorhabditis elegans.

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    <p>Abstract</p> <p>Background</p> <p>Sperm cells must regulate the timing and location of activation to maximize the likelihood of fertilization. Sperm from most species, including the nematode <it>Caenorhabditis elegans</it>, activate upon encountering an external signal. Activation for <it>C. elegans </it>sperm occurs as spermatids undergo spermiogenesis, a profound cellular reorganization that produces a pseudopod. Spermiogenesis is initiated by an activation signal that is transduced through a series of gene products. It is now clear that an inhibitory pathway also operates in spermatids, preventing their premature progression to spermatozoa and resulting in fine-scale control over the timing of activation. Here, we describe the involvement of a newly assigned member of the inhibitory pathway: <it>spe-4</it>, a homolog of the human presenilin gene PS1. The <it>spe-4(hc196) </it>allele investigated here was isolated as a suppressor of sterility of mutations in the spermiogenesis signal transduction gene <it>spe-27</it>.</p> <p>Results</p> <p>Through mapping, complementation tests, DNA sequencing, and transformation rescue, we determined that allele <it>hc196 </it>is a mutation in the <it>spe-4 </it>gene. Our data show that <it>spe-4(hc196) </it>is a bypass suppressor that eliminates the need for the spermiogenesis signal transduction. On its own, <it>spe-4(hc196) </it>has a recessive, temperature sensitive spermatogenesis-defective phenotype, with mutants exhibiting (i) defective spermatocytes, (ii) defective spermatids, (iii) premature spermatid activation, and (iv) spermatozoa defective in fertilization, in addition to a small number of functional sperm which appear normal microscopically.</p> <p>Conclusion</p> <p>A fraction of the sperm from <it>spe-4(hc196) </it>mutant males progress directly to functional spermatozoa without the need for an activation signal, suggesting that <it>spe-4 </it>plays a role in preventing spermatid activation. Another fraction of spermatozoa from <it>spe-4(hc196) </it>mutants are defective in fertilization. Therefore, prematurely activated spermatozoa may have several defects: we show that they may be defective in fertilization, and earlier work showed that they obstruct sperm transfer from males at mating. <it>hc196 </it>is a hypomorphic allele of <it>spe-4</it>, and its newly-discovered role inhibiting spermiogenesis may involve known proteolytic and/or calcium regulatory aspects of presenilin function, or it may involve yet-to-be discovered functions.</p

    Co-evolution of male and female reproductive traits across the Bruchidae (Coleoptera)

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    1. Despite the obvious importance of spermatozoa to individual reproductive success a general explanation of variation in spermatozoan form and function is still lacking. In species with internal fertilization, sperm not only have to interact with the physical and biochemical environment of the female reproductive tract, but frequently face competition from the sperm of rival males. Both sperm competition theory and adaptation to the selective environment of the female reproductive tract have been implicated in the evolution of spermatozoan morphological diversity. 2. Using the comparative method, we examine variation in sperm length in relation to (i) sperm competition intensity (as measured by relative testis size) and (ii) female reproductive characters, across 15 species of beetle belonging to the family Bruchidae. 3. Stepwise multiple regression within a phylogenetic framework revealed sperm length to be positively correlated with female spermathecal duct length and negatively related to spermathecal volume, but not testes size, indicating that the female reproductive environment rather than sperm competition per se exerts selection on sperm length in this taxonomic group. 4. A positive association between testes volume and the volume of the female spermatheca was also evident suggesting correlated evolution of these traits. 5. A number of models of sexual selection could lead to the correlated evolution of male and female reproductive characters, although the underlying mechanisms of cause and effect remain elusive. Divergence between species (and populations) in primary reproductive traits is likely to present a significant barrier to hetero-specific fertilization, and thus contribute to reproductive isolation

    An Economic History of Ellis County, Kansas

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    Like many American rural communities in the second decade of the twenty-first century, Ellis County faces tough decisions regarding economic development, population growth, and sustainable strategies. This paper examines the history of the region since the early twentieth century, tracing the evolution of various industries—from oil to farming—and the different ways the community responded to the area and nation’s economic shifts. This “big picture” view of Ellis County operates as a starting point for strategizing paths forward for area residents

    A persistent mitochondrial deletion reduces fitness and sperm performance in heteroplasmic populations of C. elegans

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    BACKGROUND: Mitochondrial DNA (mtDNA) mutations are of increasing interest due to their involvement in aging, disease, fertility, and their role in the evolution of the mitochondrial genome. The presence of reactive oxygen species and the near lack of repair mechanisms cause mtDNA to mutate at a faster rate than nuclear DNA, and mtDNA deletions are not uncommon in the tissues of individuals, although germ-line mtDNA is largely lesion-free. Large-scale deletions in mtDNA may disrupt multiple genes, and curiously, some large-scale deletions persist over many generations in a heteroplasmic state. Here we examine the phenotypic effects of one such deletion, uaDf5, in Caenorhabditis elegans (C. elegans). Our study investigates the phenotypic effects of this 3 kbp deletion. RESULTS: The proportion of uaDf5 chromosomes in worms was highly heritable, although uaDf5 content varied from worm to worm and within tissues of individual worms. We also found an impact of the uaDf5 deletion on metabolism. The deletion significantly reduced egg laying rate, defecation rate, and lifespan. Examination of sperm bearing the uaDf5 deletion revealed that sperm crawled more slowly, both in vitro and in vivo. CONCLUSION: Worms harboring uaDf5 are at a selective disadvantage compared to worms with wild-type mtDNA. These effects should lead to the rapid extinction of the deleted chromosome, but it persists indefinitely. We discuss both the implications of this phenomenon and the possible causes of a shortened lifespan for uaDf5 mutant worms

    Knockout of the folate transporter folt-1 causes germline and somatic defects in C. elegans

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    <p>Abstract</p> <p>Background</p> <p>The <it>C. elegans </it>gene <it>folt-1 </it>is an ortholog of the human reduced folate carrier gene. The FOLT-1 protein has been shown to transport folate and to be involved in uptake of exogenous folate by worms. A knockout mutation of the gene, <it>folt-1(ok1460)</it>, was shown to cause sterility, and here we investigate the source of the sterility and the effect of the <it>folt-1 </it>knockout on somatic function.</p> <p>Results</p> <p>Our results show that <it>folt-1(ok1460) </it>knockout hermaphrodites have a substantially reduced germline, generate a small number of functional sperm, and only rarely produce a functional oocyte. We found no evidence of increased apoptosis in the germline of <it>folt-1 </it>knockout mutants, suggesting that germline proliferation is defective. While <it>folt-1 </it>knockout males are fertile, their rate of spermatogenesis was severely diminished, and the males were very poor maters. The mating defect is likely due to compromised metabolism and/or other somatic functions, as <it>folt-1 </it>knockout hermaphrodites displayed a shortened lifespan and elongated defecation intervals.</p> <p>Conclusions</p> <p>The FOLT-1 protein function affects both the soma and the germline. <it>folt-1(ok1460) </it>hermaphrodites suffer severely diminished lifespan and germline defects that result in sterility. Germline defects associated with folate deficiency appear widespread in animals, being found in humans, mice, fruit flies, and here, nematodes.</p
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