18 research outputs found
Transgenerational Effects of Parental Larval Diet on Offspring Development Time, Adult Body Size and Pathogen Resistance in Drosophila melanogaster
Environmental conditions experienced by parents are increasingly recognized to affect offspring performance. We set out to investigate the effect of parental larval diet on offspring development time, adult body size and adult resistance to the bacterium Serratia marcescens in Drosophila melanogaster. Flies for the parental generation were raised on either poor or standard diet and then mated in the four possible sex-by-parental diet crosses. Females that were raised on poor food produced larger offspring than females that were raised on standard food. Furthermore, male progeny sired by fathers that were raised on poor food were larger than male progeny sired by males raised on standard food. Development times were shortest for offspring whose one parent (mother or the father) was raised on standard and the other parent on poor food and longest for offspring whose parents both were raised on poor food. No evidence for transgenerational effects of parental diet on offspring disease resistance was found. Although paternal effects have been previously demonstrated in D. melanogaster, no earlier studies have investigated male-mediated transgenerational effects of diet in this species. The results highlight the importance of not only considering the relative contribution each parental sex has on progeny performance but also the combined effects that the two sexes may have on offspring performance
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The Exocyst Protein Sec10 Interacts with Polycystin-2 and Knockdown Causes PKD-Phenotypes
Autosomal dominant polycystic kidney disease (ADPKD) is characterized by
formation of renal cysts that destroy the kidney. Mutations in PKD1 and PKD2,
encoding polycystins-1 and -2, cause ADPKD. Polycystins are thought to function
in primary cilia, but it is not well understood how these and other proteins are
targeted to cilia. Here, we provide the first genetic and biochemical link
between polycystins and the exocyst, a highly-conserved eight-protein membrane
trafficking complex. We show that knockdown of exocyst component Sec10 yields
cellular phenotypes associated with ADPKD, including loss of flow-generated
calcium increases, hyperproliferation, and abnormal activation of MAPK. Sec10
knockdown in zebrafish phenocopies many aspects of polycystin-2
knockdown—including curly tail up, left-right patterning defects,
glomerular expansion, and MAPK activation—suggesting that the exocyst is
required for pkd2 function in vivo. We observe
a synergistic genetic interaction between zebrafish sec10 and
pkd2 for many of these cilia-related phenotypes.
Importantly, we demonstrate a biochemical interaction between Sec10 and the
ciliary proteins polycystin-2, IFT88, and IFT20 and co-localization of the
exocyst and polycystin-2 at the primary cilium. Our work supports a model in
which the exocyst is required for the ciliary localization of polycystin-2, thus
allowing for polycystin-2 function in cellular processes