The Muller F element (4.2 Mb, ~80 protein-coding genes) is an unusual autosome of Drosophila melanogaster; it is mostly heterochromatic with a low recombination rate. To investigate how these properties impact the evolution of repeats and genes, we manually improved the sequence and annotated the genes on the D. erecta, D. mojavensis, and D. grimshawi F elements and euchromatic domains from the Muller D element. We find that F elements have greater transposon density (25–50%) than euchromatic reference regions (3–11%). Among the F elements, D. grimshawi has the lowest transposon density (particularly DINE-1: 2% vs. 11–27%). F element genes have larger coding spans, more coding exons, larger introns, and lower codon bias. Comparison of the Effective Number of Codons with the Codon Adaptation Index shows that, in contrast to the other species, codon bias in D. grimshawi F element genes can be attributed primarily to selection instead of mutational biases, suggesting that density and types of transposons affect the degree of local heterochromatin formation. F element genes have lower estimated DNA melting temperatures than D element genes, potentially facilitating transcription through heterochromatin. Most F element genes (~90%) have remained on that element, but the F element has smaller syntenic blocks than genome averages (3.4–3.6 vs. 8.4–8.8 genes per block), indicating greater rates of inversion despite lower rates of recombination. Overall, the F element has maintained characteristics that are distinct from other autosomes in the Drosophila lineage, illuminating the constraints imposed by a heterochromatic milieu.

13Local accumulation of oskar (osk) mRNA in the Drosophila oocyte 14 determines the posterior pole of the future embryo. Two major cytoskeletal 15 components, microtubules and actin filaments, together with a microtubule motor, 16 kinesin-1, and an actin motor, myosin-V, are essential for osk mRNA posterior 17 localization. In this study, we use Staufen, an RNA-binding protein that 18 colocalizes with osk mRNA, as a proxy for osk mRNA. We demonstrate that 19 posterior localization of osk/Staufen is determined by competition between 20 2 kinesin-1 and myosin-V. While kinesin-1 removes osk/Staufen from the cortex 21 along microtubules, myosin-V anchors osk/Staufen at the cortex. Myosin-V wins 22 over kinesin-1 at the posterior pole due to low microtubule density at this site, 23 while kinesin-1 wins at anterior and lateral positions because they have high 24 density of cortically-anchored microtubules. As a result, posterior determinants 25 are removed from the anterior and lateral cortex but retained at the posterior pole. 26 Thus, posterior determination of Drosophila oocytes is defined by kinesin-myosin 27 competition, whose outcome is primarily determined by cortical microtubule 28 density. 29 Staufen mislocalization than the ectopic expression of Khc ΔHinge2 in the Khc null 128 background from a previous study 36 . Intriguingly, later in development (at stage 129 10B) normal Staufen distribution is recovered with the restoration of the posterior 130 cap and clearing of the central cytoplasmic aggregate (Figure 1F-1H; Figure 1-131 figure supplement 1F,1H,1J). Previous studies suggest that Osk protein, 132 translated at the posterior pole, functions in a positive feedback mechanism for 133 osk/Staufen accumulation in streaming oocytes 10, 37 . We postulate that enough 134 Osk protein translates from the residual cap, initiating the positive feedback loop, 135 while ooplasmic streaming circulates mislocalized osk/Staufen particles to the 136 posterior cap, enhancing Osk localization, resulting the restoration of the 137 posterior crescent. 138 Together, our data show that osk/Staufen posterior localization is sensitive 139 to kinesin-1 activity level.140 141 Staufen localization is controlled by myosin-V 142 If osk/Staufen localization is indeed controlled by kinesin-myosin 143 competition, a change of myosin-V activity would be predicted to disrupt 144 osk/Staufen posterior localization. Previous studies reveal that inhibition of 145 myosin-V by overexpression of the C-terminal myosin-V globular tail (GT) causes 146 Staufen mislocalization to the center of the oocyte 5, 10 , which is in agreement with 147 our hypothesis that myosin-V anchors osk/Staufen at the posterior cortex. In 148 addition, our hypothesis predicts that increased myosin-V activity alters the 149 plugins (Curvetracing, Steger's algoristhm, developed in Cell Biology group of 595 Utrecht University by Jalmar Teeuw and Eugene Katrukha) and the length of all 596 traced lines was measured. The total length of all traced microtubules lines 597...

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Ventral furrow formation, the first step in Drosophila gastrulation, is a well-studied example of tissue morphogenesis. Rho1 is highly active in a subset of ventral cells and is required for this morphogenetic event. However, it is unclear whether spatially patterned Rho1 activity alone is sufficient to recapitulate all aspects of this morphogenetic event, including anisotropic apical constriction and coordinated cell movements. Here, using an optogenetic probe that rapidly and robustly activates Rho1 in Drosophila tissues, we show that Rho1 activity induces ectopic deformations in the dorsal and ventral epithelia of Drosophila embryos. These perturbations reveal substantial differences in how ventral and dorsal cells, both within and outside the zone of Rho1 activation, respond to spatially and temporally identical patterns of Rho1 activation. Our results demonstrate that an asymmetric zone of Rho1 activity is not sufficient to recapitulate ventral furrow formation and reveal that additional, ventral-specific factors contribute to the cell- and tissue-level behaviors that emerge during ventral furrow formation.

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