Germline
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Germline regulation of tumor evolutionary dynamics shapes multiple myeloma progression
Germline variation shapes cancer risk, yet its influence on the evolutionary dynamics of established tumors remains poorly understood. In multiple myeloma, subclonal diversification drives disease progression and treatment failure, but the heritable factors that modulate this process are unknown. Here, we show that germline variation is associated with tumor evolutionary features, implicating inherited regulation in subclonal expansion.
Genetic control of mitotic-to-meiotic transition regulates germline cell survival
The coordination between DNA damage repair and cell cycle progression is essential to ensure cell survival and organ homeostasis. This is particularly critical during gametogenesis, where germline cells first proliferate and then transition from mitosis to meiosis. Meiotic cells frequently undergo recombination, which itself implies the generation of severe DNA damage in the form of double-strand DNA breaks (DSBs) that ought to be repaired to preserve genome integrity.
Somatic cells non-autonomously control germline incomplete cytokinesis through FGF signaling
Across species, germ cells divide and differentiate as interconnected units, termed cysts. These cysts are generated through reiterative rounds of mitosis followed by incomplete cytokinesis to generate stable ring canals (RCs). Despite the ubiquity of germ cell incomplete cytokinesis, it is still unclear how this program is mechanistically regulated across multiple cell cycles to promote integrity of the cyst.
Functional Characterization of Myeloid Neoplasm-associated DDX41 Variants Reveals Pathogenic Interaction with Acquired Hotspot Mutation
Germline variants in DDX41 are the most frequent genetic predisposition to adult hematologic malignancies. The most common variants are truncating, implicating loss of function in the pathogenesis. However, non-truncating variants account for 30-40% of cases, and their impact on essential DDX41 functions remains unknown.
Genotype and methylation interact to reconfigure transcriptional regulation in colorectal cancer
Background Transcriptional regulation is shaped by both genomic variants and the environment. Yet, how the regulatory effects of genomic variants are reconfigured by dynamic epigenomic changes during tumorigenesis remains incompletely understood. Methods We investigated methylation context-dependent links between genotype and gene expression in colorectal cancer (CRC) using paired tumor and normal-adjacent tissue (NAT) from 80 patients, thereby controlling for germline genomic background.
The people who actually want AI to replace humanity
“I want AI to be a tool that allows human flourishing!” exclaimed Brad Carson, a former member of Congress. “There is an option out there where AI is just a tool for us.” The people who actually want AI to replace humanity We need to create a new humanism before the “AI successionists” win.
Q&A: Why do telomeres shorten when a cell divides, and how does it affect human aging?
Q&A: Why do telomeres shorten when a cell divides, and how does it affect human aging? Stephanie Baum Scientific Editor Andrew Zinin Lead Editor In each cell of your body, DNA is stored in structures called chromosomes.
Are we getting to the point where it's safe to gene-edit babies?
When a rogue researcher in China revealed in 2018 that he had used CRISPR to create three gene-edited children, his actions were almost universally condemned by biologists around the world. The main objection was not that gene-editing babies is wrong in itself, but that the CRISPR technique used was not safe and had a very high risk of causing harmful mutations. Now, a team in the US has used an improved form of CRISPR, known as base editing, to edit healthy embryos and shown that it can be...
Modes of natural selection on maternal and zygotic gene expression in Drosophila melanogaster embryos
Early embryonic development involves the coordination of gene expression from two distinct genomes, as mothers load eggs with gene products prior to the beginning of zygotic transcription. Because the maternal transcriptome is controlled by the mothers regulatory genotype rather than that of the embryo, these two sequential developmental programs may experience distinct evolutionary constraints and selection pressures despite both existing within the embryo. To infer modes of selection on...
Mutation-dependent responses to sleep and exercise in clonal haematopoiesis
Abstract Clonal haematopoiesis (CH) activates inflammation and increases the risk of atherosclerosis1,2. Whether lifestyle alters CH clone expansion or the phenotypic programming of CH mutant cells, thereby affecting atherosclerosis, is unknown. Here, in humans and mice and across mutations in Jak2, Tet2, Trp53 and Dnmt3a, we demonstrate mutation-dependent responses to sleep and exercise in CH and show that mutant cells are uniquely sensitive to lifestyle.