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Aigaki, T.

Publications and source records attributed to Aigaki, T..

3 recordsLinked to original sources

Resilin, the gene for the molecular spring: its roles in the flight and jumpingof Drosophila

Resilin is a member of the chitin-binding protein family that was originally found as a major component of an elastic matrix present in insects. The knockdown of the gene for this protein in Drosophila melanogaster causes the characteristic downturned wing posture, and the knockdown flies cannot move their wings. The jump distance of the knockdown flies is around 50% shorter than that of the controls. Null mutant flies show the same phenotypes, which can be rescued by introducing a 4.7 kb genomic fragment harboring the whole coding region of Resilin. In vitro experiments have shown that the elasticity of the matrix made of Resilin is due to the dityrosine-mediated polymerization of Resilin molecules. Dual oxidase (Duox) is the most likely candidate for the in vivo polymerization of Resilin molecules. Duox knockdown induces phenotypes similar to those observed in wing posture and jump performance of the Resilin knockdown and knockout flies, which can be rescued by the overexpression of Duox gene from a beetle. These findings suggest that Duox is an essential factor for the proper function of Resilin as the major component of the resilin matrix.

genetics↗

The Drosophila AWP1 ortholog Doctor No regulates JAK/STAT signaling for left-right asymmetry in the gut by promoting receptor endocytosis

Many internal Drosophila organs show stereotypical left-right (LR) asymmetry, for which the underlying mechanisms remain elusive. Here, we identified an evolutionarily conserved ubiquitin-binding protein, AWP1/Doctor no (Drn), as a novel factor required for the LR asymmetry of the embryonic anterior gut in Drosophila. We showed that drn is essential in the circular visceral muscle cells of the midgut for JAK/STAT signaling, which contributes to the first known cue for anterior gut lateralization via LR-asymmetric nuclear rearrangement. Embryos homozygous for drn and lacking its maternal contribution showed phenotypes similar to that of depleted JAK/STAT signaling, suggesting that Drn is a general component of JAK/STAT signaling. The absence of Drn resulted in the specific accumulation of Domeless (Dome), the receptor of JAK/STAT signaling, in intracellular compartments. Thus, Drn is required for the endocytic trafficking of Dome, which is subsequently degraded in lysosomes. Our results suggest that the endocytosis of Dome is a critical step in activating JAK/STAT signaling. The roles of AWP1/Drn in activating JAK/STAT signaling and in LR-asymmetric development may be conserved in various organisms. Summary StatementDr. No, a Drosophila ortholog of AWP1, activates JAK/STAT signaling via Dome receptor endocytosis in a crucial step for left-right asymmetry in the developing gut.

developmental biology↗

Sir2 is essential for intergenerational effects of parental diet on offspring metabolism in Drosophila

Recent studies have revealed that parental diet can affect offspring metabolism and longevity in Drosophila. However, the underlying mechanisms are still unknown. Here we demonstrate that Sir2 encoding an NAD+-dependent histone deacetylase is required for the intergenerational effects of low nutrition diet (1:5 dilution of standard diet). We observed an increased amount of triacylglyceride (TAG) in the offspring when fathers were maintained on a low nutrition diet for 2 days. The offspring had increased levels of metabolites of glycolysis and TCA cycle, the primary energy producing pathways. We found that Sir2 mutant fathers showed no intergenerational effects. RNAi-mediated knockdown of Sir2 in the fat body was sufficient to mimic the Sir2 mutant phenotype, and the phenotype was rescued by transgenic expression of wild-type Sir2 in the fat body. Interestingly, even fathers had no experience of low nutrition diet, overexpression of Sir2 in their fat bodies induced a high level of TAG in the offspring. These findings indicated that Sir2 is essential in the fat body of fathers to induce intergenerational effects of low nutrition diet.

genetics↗