Mobilization of the P family of transposable elements in Drosophila melanogaster occurs in the hybrid progeny of males from an element-bearing strain (P strain) and females from an element-free strain (M strain). We tested whether the same crosses could mobilize other families of transposable elements. A mating scheme was used in which a set of X chromosomes was kept for 20 generations in either the active condition (known as hybrid dysgenesis) or the inactive condition (nondysgenic). Examination of 19 families of transposable elements by in situ hybridization indicated that only the P family was measurably mobilized under dysgenic conditions. Thus, P-M hybrid dysgenesis does not increase the transpositional activity of other families of transposable elements in D. melanogaster. We discuss possible explanations for several published reports to the contrary.
Microtubules are essential to neuron shape and function. Therefore, the stability of the microtubule cytoskeleton must be carefully regulated. Acetylation of tubulin has the potential to directly tune microtubule stability, and proteomic studies have identified several acetylation sites in α-tubulin. This includes the highly conserved residue lysine 394 (K394), which is located at the αβ-tubulin dimer interface. Using a fly model, we show that α-tubulin K394 is acetylated in the nervous system and is an essential residue. We found that an acetylation-blocking mutation in endogenous α-tubulin, K394R, perturbs the synaptic morphogenesis of motoneurons by reducing microtubule stability. Intriguingly, the K394R mutation has opposite effects on the growth of two functionally and morphologically distinct motoneurons, revealing neuron-type-specific responses when microtubule stability is altered. Eliminating the deacetylase HDAC6 increases K394 acetylation, and the over-expression of HDAC6 reduces microtubule stability similar to the K394 mutant. Thus, our findings implicate α-tubulin K394 and its acetylation in the regulation of microtubule stability and suggest that HDAC6 regulates K394 acetylation during synaptic morphogenesis.
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