We had an incredible time at our recent departmental retreat! A big thank you to everyone in the lab for making it such a memorable and enjoyable experience.
Posts
🚲🚲 2023 Team Buckeyes! 🚲🚲
DNA double-strand breaks induce H2Ax phosphorylation domains in a contact-dependent manner
(picture from from H2Ax wikipedia)
New Paper in Nature Communications! “DNA double-strand breaks induce H2Ax phosphorylation domains in a contact-dependent manner” Collins et al, 2020
Ever wonder how DNA damage foci know how big to get? Find out!
Enhanced epigenetic profiling of classical human monocytes reveals a specific signature of healthy aging in the DNA methylome
New Paper in Nature Aging! Enhanced epigenetic profiling of classical human monocytes reveals a specific signature of healthy aging in the DNA methylome
The impact of healthy aging on molecular programming of immune cells is poorly understood. Here we report comprehensive characterization of healthy aging in human classical monocytes, with a focus on epigenomic, transcriptomic and proteomic alterations, as well as the corresponding proteomic and metabolomic data for plasma, using healthy cohorts of 20 young and 20 older males (~27 and ~64 years old on average). For each individual, we performed enhanced reduced representation bisulfite sequencing-based DNA methylation profiling, which allowed us to identify a set of age-associated differentially methylated regions (DMRs)—a novel, cell-type-specific signature of aging in the DNA methylome. Hypermethylation events were associated with H3K27me3 in the CpG islands near promoters of lowly expressed genes, while hypomethylated DMRs were enriched in H3K4me1-marked regions and associated with age-related increase of expression of the corresponding genes, providing a link between DNA methylation and age-associated transcriptional changes in primary human cells.
(picture from pintrest.com)
Blood natural killer cell deficiency reveals an immunotherapy strategy for atopic dermatitis
New paper in Science Translational Medicine!
We find that a subset of natural killer cells are absent in the blood of patients with atopic dermatitis (AD), an autoimmune skin disorder. Moreover, this cellular deficiency can separate AD from other similar diseases, and may represent a therapy target.
Blood natural killer cell deficiency reveals an immunotherapy strategy for atopic dermatitis
Madison R. Mack, Jonathan R. Brestoff, Melissa M. Berrien-Elliott, Anna M. Trier1, Ting-Lin B. Yang, Matthew McCullen, Patrick L. Collins, Haixia Niu, Nancy D. Bodet, Julia A. Wagner, Eugene Park, Amy Z. Xu, Fang Wang, Rebecca Chibnall, M. Laurin Council, Carrie Heffington, Friederike Kreisel, David J. Margolis, David Sheinbein, Paola Lovato, Eric Vivier, Marina Cella, Marco Colonna, Wayne M. Yokoyama, Eugene M. Oltz, Todd A. Fehnigher and Brian S. Kim
Barrier-to-Autointegration Factor 1 Protects against a Basal cGAS-STING Response
The cell needs to regulate the antiviral response in order to maintain cellular homeostasis. Here we identify as non-specific DNA binding protein, BANF1, as a mechanism that modulates their basal levels of the dsDNA mediated anti-viral response.
Barrier-to-Autointegration Factor 1 Protects against a Basal cGAS-STING Response
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Regional Gene Repression by DNA Double-Strand Breaks in G1 Phase Cells
The origin of many, if not all, cancers can be traced back to an initial DNA damaging event. Surprisingly, these events are common. Indeed, gene transcription itself can cause damage through metabolic byproducts or toxic DNA-RNA hybrids. Here we show that a DSB will activate machinery that suppresses further transcription a long way along the chromatin fiber, perhaps to stop more damage.
Regional Gene Repression by DNA Double-Strand Breaks in G1 Phase Cells
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Circadian rhythm–dependent and circadian rhythm–independent impacts of the molecular clock on type 3 innate lymphoid cells
The circadian clock controls our 24-hour biological cycles, including immunity. This machinery is within every cell, yet directly interfaces with only a subset of biological functions. We find that one component controls type three innate lymphocytes, which are our rapid responders to bacteria
Qianli Wang, Michelle L. Robinette, Cyrielle Billon, Patrick L. Collins, Jennifer K. Bando, José LuÃs Fachi, Cristiane Sécca1, Sofia I. Porter, Ankita Saini, Susan Gilfillan, Laura A. Solt, Erik S. Musiek, Eugene M. Oltz, Thomas P. Burris and Marco Colonna
Current focuses:
A) the genomic regulators of human innate lymphocytes, which provide surveillance for metastasis and clear hematological malignancies; and
B) the mechanisms that stabilize DNA breaks during adaptive lymphocyte development, and thereby prevent end disassociation and oncogenic recombination.
Funding:
Department of Microbial Infection and Immunity Pilot Grant
Contact:
Patrick.Collins@osumc.edu