Molecular dynamics (MD) simulations provide a molecularresolution view of biomolecular folding and assembly processes, but the computational demands of the underlying algorithms limit the lenth-and time-scales of the simulations one can perform. Recently, graphics processing units (GPUs), specialized devices that were originally designed for rendering images, have been repurposed for high performance computing, and there have been significant increases in the performances of parallel algorithms such as the ones in MD simulations. Previously, we implemented a GPUoptimized parallel neighbor list algorithm for our coarsegrained MD simulations, and we observed an N -dependent speed-up (or speed-down) compared to a CPU-optimized algorithm, where N is the number of interacting beads representing amino acids or nucleotides for proteins or RNAs, respectively. We had demonstrated that for MD simulations of the 70s ribosome (N =10,219), our GPU-optimized code was about 30x as fast as a CPU-optimized version. In our present study, we implement a hybrid neighbor/cell list algorithm that borrows components from the well-known neighbor list and the cell-list algorithms. We observe about 10% speedup as compared to our previous implementation of a GPU-optimized parallel neighbor list algorithm.

The Janus-kinase/Signal Transducers and Activators of Transcription (JAK/STAT) pathway regulates the anterior posterior axis of the Drosophila follicle cells. In the anterior, it activates the bone morphogenetic protein (BMP) signaling pathway through expression of the BMP ligand, decapentaplegic (dpp). In the posterior, JAK/STAT works with the epidermal growth factor receptor (EGFR) pathway to express the T-box transcription factor midline (mid). While MID is necessary in establishing the posterior fate of the egg chamber, we show that it is not sufficient to determine a posterior fate. The ETS-transcription factor pointed (pnt) is expressed in an overlapping domain to mid in the follicle cells. This study shows that pnt is upstream of mid, and it is sufficient to induce a posterior fate in the anterior end, which is characterized by the induction of mid, the prevention of the stretched cells formation, and the abrogation of border cells migration. We demonstrate that the anterior BMP signaling is abolished by PNT through dpp repression. However, ectopic DPP cannot rescue this repression, suggesting additional targets of PNT participate in the posterior fate determination.

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The posterior end of the follicular epithelium is patterned by midline (MID) and its paralog H15, the Drosophila homologs of the mammalian Tbx-20 transcription factor. We previously identified two cis-regulatory modules (CRMs) that recapitulate the endogenous pattern of mid in the follicular epithelium. Here, through CRISPR/Cas9 genome editing, we demonstrate redundant activity of these mid CRMs. While the deletion of either CRM alone generated marginal change in mid expression, the deletion of both CRMs reduced expression by 60%. Unexpectedly, the deletion of the 5’ proximal CRM of mid eliminated H15 expression. Interestingly, expression of these paralogs in other tissues remained unaffected in the CRMs deletion backgrounds. These results suggest that the paralogs are regulated by a shared-CRM that coordinates gene expression during posterior fate determination. The consistent overlapping expression of mid and H15 in various tissues may indicate that the paralogs could also be under shared regulation by other CRMs in these tissues.