Project description:This SuperSeries is composed of the following subset Series: GSE31344: smRNA sequencing of queen and virgin queen of two ants: Camponotus floridanus and Harpegnathos saltator GSE31346: Transcriptome sequencing of queen and virgin queen of two ants: Camponotus floridanus and Harpegnathos saltator GSE31576: Single base resolution methylome of two ants: Camponotus floridanus and Harpegnathos saltator Refer to individual Series
Project description:Neurons in posterior parietal cortex contribute to the execution of goal-directed navigation and other decision-making tasks. Although molecular studies have catalogued over fifty cortical cell types, it remains unknown what distinct functions they serve during goal-directed navigation. Here, we identified a molecularly defined subset of somatostatin (Sst) inhibitory neurons that, in mouse posterior parietal cortex, carry a novel cell type-specific error correction signal for navigation. We obtained repeatable experimental access to these cells using an adeno-associated virus (AAV) in which gene expression is driven by an enhancer that functions specifically in a subset of Sst cells. We found that during goal-directed navigation in a virtual environment, this subset of Sst neurons activates in a synchronous pattern that is distinct from the activity of surrounding neurons, including other Sst neurons. Using in vivo two-photon photostimulation and ex vivo paired patch clamp recordings, we show that nearby cells of this Sst subtype excite each other through gap junctions, revealing a self-excitation circuit motif that contributes to the synchronous activity of this cell type. Remarkably, these cells selectively activate as mice execute course corrections for deviations in their virtual heading during navigation toward a reward location, both for self- and experimentally-induced deviations. We propose that this subtype of Sst neurons provides a self-reinforcing and cell type-specific error-correction signal in posterior parietal cortex that may aid the execution and learning of accurate goal-directed navigation trajectories.
Project description:The goal of this study was to assay the extent of variation in chromatin organization between 3 ant castes (major and minor female workers and males) in one colony of Camponotus floridanus carpenter ant using ChIPseq. 45 samples total: 30 ChIP samples and 3 inputs for total histone H3, 7 histone H3 PTMs and RNA Pol II in major, minor, and male ants; CBP in major and minor ants; the major H3K27ac sample was replicated. 4 ChIP samples for H3 and H3K27ac in brains of majors and minors, and 2 inputs. 2 RNAseq samples for major and minor ants head+thorax; 4 RNAseq samples for brain (majors and minors with 2 replicates each).
Project description:This SuperSeries is composed of the following subset Series: GSE22678: Transcriptome sequencing and analysis of two ants: Camponotus floridanus and Harpegnathos saltator GSE22679: Small RNA sequencing and analysis of two ants: Camponotus floridanus and Harpegnathos saltator Refer to individual Series
Project description:High tumor mutational burden (TMB) is a predictive biomarker for the responsiveness of cancer to immune checkpoint inhibitor therapy that indicates whether immune cells can sufficiently recognize cancer cells as non-self. However, about 30% of all cancers from The Cancer Genome Atlas are classified as immune-desert tumors lacking T cell infiltration despite high TMB. Since the underlying mechanism of these immune-desert tumors has yet to be unraveled, there is a pressing need to transform such immune-desert tumors into immune-inflamed tumors and thereby enhance their responsiveness to anti-PD1 therapy. Here, we present a systems framework for identifying immuno-oncotargets, based on analysis of gene regulatory networks, and validating the effect of these targets in transforming immune-desert into immune-inflamed tumors. In particular, we identify DEAD-box helicases 54 (DDX54) as a master regulator of immune escape in immune-desert lung cancer with high TMB, and show that knockdown of DDX54 can increase immune cell infiltration and lead to improved sensitivity to anti-PD1 therapy.