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Comparative analysis establishes genetic links among angioimmunoblastic T-cell lymphoma (AITL), clonal hematopoiesis, and concomitant hematologic malignancies, and provides insights into the cell of origin, etiology, and biomarker discovery for AITL.

Genetic variation can have multiple effects on different phenotypic traits in organisms living in the natural environment.

Isw1 acts as a master regulator in modulating the expression of drug-resistance genes, and this regulatory mechanism is dependent on the interaction of Isw1 acetylation and ubiquitination.

Horizontal gene transfer (HGT) helps slightly beneficial genes persist in microbial populations, incentivising cells to invest in costly DNA uptake, even in the presence of harmful selfish genetic elements.

The splicing factor RNP-6/PUF60 suppresses immunity by modulating host splicing and transcriptional responses to infection.

In contrast with earlier conclusions, negative selection has a major role in cancer evolution.

The genetic background of a cancer cell and the chromatin organization of the tissue-of-origin impact the amount, length and position of somatic copy number alterations in cancer.

Plexin controls the spatial distribution of synapses by locally inhibiting Rap2 small GTPase activity along the axon, and a Rap2 effector, TNIK, which also plays a key role in inhibiting synapse number.

The pseudokinase Tribbles1 is expressed in human monocytes after mycobacterial challenge and can be manipulated to be host protective against mycobacterial infection, due to control of innate immune cell function, in a zebrafish tuberculosis model.

Monosomy in yeast results in numerous gene dosage insufficiencies with potentially lethal collective effect, but strong positive epistasis rooted in the modular structure of cell metabolism cancels it.