Browse our latest Genetics and Genomics articles

Quantification of both viral transcription and progeny production from single influenza-infected cells shows that the cells that produce the most viral RNA often do not produce the most virions.

CD8+ Trm cells' erosion role in oral lichen planus via IFN-γ, TNF-α, and IL17 cytokines has been revealed, addressing a gap in recurrent erosion studies.

Increased production of ether lipids is required to extend lifespan in response to metformin, phenformin, and multiple, distinct, longevity-promoting manipulations, illuminating the possibility that raising ether lipid levels represents a new therapeutic strategy to support healthy aging.

How biologically relevant chemical information can be genetically maintained and conveyed in complex sex pheromonal profiles.

The long-range resection machinery is dispensable for homologous recombination between closely linked repeats but is necessary for DNA damage checkpoint activation which is associated with interchromosomal recombination.

Combining computational and experimental approaches reveals that the loss of a maternal transcription factor influences sex-biased differential splicing in the early zygotic transcriptome at genes that are critical for normal developmental processes.

SUMOylated PCNA and the Elg1 PCNA unloader interact with the CST complex to coordinate DNA replication and telomere length maintenance.

The transcriptional cofactor HPK-1 (homeodomain-interacting protein kinase) functions as a key regulator of multiple proteostatic stress responses, each originating from discrete neuronal subtypes within the Caenorhabditis elegans nervous system to preserve neuronal health and maintain organismal proteostasis during normal aging.

Continuing advances in functional genomics will enable systematic characterization of how non-coding genetic variation at enhancers impacts developmental diseases.

A genetic screen identifies a lipid pathway which impacts the endoplasmic reticulum unfolded protein response and highlights a mechanism through which lipid disequilibrium might facilitate the progression of proteopathic diseases.