The latest discoveries in Genetics
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How the fasting gut tells the brain to hold back on protein
This Cell study identifies a gut–brain signaling pathway that curbs protein intake during recovery from severe fasting. Ammonia generated from the metabolism of particular dietary amino acids is sensed by Trpa1-positive intestinal epithelial cells, which in turn activate neural circuits that promote aversion to protein-rich foods. The work links a specific metabolic byproduct to a defined sensory cell population and behavioral output, offering a mechanistic account of how the body temporarily restrains protein consumption after extreme energy deprivation.
Why it might matter to you: The delineated ammonia–Trpa1 axis adds a concrete, molecularly defined gut–brain mechanism that could modulate nutrient preference across individuals or genetic backgrounds. For population-based and pharmacogenomic studies, this suggests candidate pathways where genetic variation might shape diet, metabolic risk, and potentially drug handling in states of malnutrition or intensive nutritional support.
Neural fields sharpen a standard model of white-matter microstructure
The Communications Biology paper introduces a self-supervised implicit neural representation framework for estimating parameters of the Standard Model of white matter from diffusion MRI. By learning a continuous representation of the signal, the approach improves parameter fitting under noisy conditions, supports spatial upsampling, and incorporates correction for gradient non-uniformity directly into the model. This yields more precise and robust microstructural estimates without the need for explicit ground-truth labels or heavy supervision.
Why it might matter to you: More accurate and scalable estimation of white-matter microstructure can enhance genotype–phenotype mapping in imaging genetics and large population cohorts. For pharmacogenomic or neurogenetic work, these improved quantitative traits may serve as more sensitive endophenotypes when linking genetic variation to brain connectivity, treatment response, or neurotoxicity profiles.
DNA repair kinase shapes oncogenic signaling and microglial activation
This PNAS article reports that ATM kinase, best known for orchestrating DNA damage responses, also interacts with the ER chaperone GRP94 to regulate oncogenic receptor expression and downstream signaling, including effects on microglial activation. By modulating how GRP94 handles specific client proteins, ATM influences receptor abundance at the cell surface and alters inflammatory and tumor-associated signaling cascades. The findings expand ATM’s functional footprint from genome surveillance into the control of cell–cell communication within tumor and neural microenvironments.
Why it might matter to you: ATM–GRP94 crosstalk suggests additional molecular nodes where germline or somatic variation could shape cancer risk, progression, and treatment response beyond canonical DNA repair pathways. For translational genetics and pharmacogenomics, these results highlight a potential route by which ATM variants might influence sensitivity to targeted therapies or immunomodulatory agents through altered receptor expression and microglial or immune activation.