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PNAS Papers on Sea Anemone Stinging Cell Development, HIV Recombination, Mouse Embryogenesis

University of Florida researchers examine the developmental and regulatory programs behind cnidocyte stinging cells in the Nematostella vectensis sea anemone, a member of the Cnidaria phylum. With the help of gene knockdown and other functional genomic experiments, the team narrowed in on a ZNF845 zinc finger transcription factor that appears to dial down neural development in RFamide-expressing neurons, while boosting cnidocyte stinging cells. The transcription factor "coordinates both the gain of novel (cnidocyte-specific) traits and the inhibition of ancestral (neural) traits during cnidocyte development," the authors write, noting that this regulatory gene appears to have resulted from domain shuffling in the most recent shared cnidarian ancestor. "This finding is evidence that stinging cells evolved from a specific subtype of neurons and suggests other neuronal subtypes may have been coopted for other novel secretory functions," the authors write.

A team from Western University and the University of Edinburgh outlines a computational method for reconstructing genome recombination in HIV-1, focusing on isolates from the predominate group M type — an approach the researchers used to find recombination events and recombination hotspots in simulated or real HIV-1 genome sequences. "The prevailing abundance of full-length HIV type 1 (HIV-1) genome sequences provides an opportunity to revisit the standard model of HIV-1 group M (HIV-1/M) diversity that clusters genomes into largely non-recombinant subtypes," the authors write, explaining that "we develop an unsupervised nonparametric clustering approach, which does not rely on predefined nonrecombinant genomes, by adapting a community detection method developed for dynamic social network analysis."

Northwestern University researchers describe ties between histone acetylation and embryogenesis in a mouse model of the process. Using a CRISPR-Cas9-based synthetic lethal screening approach, the team demonstrated that a histone acetylation complex component encoded by ING5 can contribute to embryonic stem cell viability and development-related gene expression through interactions with catalytically inactive forms of the SET1 (COMPASS) histone 3 lysine 4 methyltransferase complex — a histone modification pathway that typically seems to influence mouse embryogenesis through Set1A's catalytic domain. "Taken together, our results point toward Set1A/COMPASS and ING5 as potential coregulators of the self-renewal and differentiation status of [embryonic stem cells]," the authors note

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