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Conserved transcriptomic profile of uropathogenic E. coli in patients identifies an infection-specific metabolic state.

An orphan TBP-associated factor, TAF9B, works in conjunction with the histone acetyl-transferase PCAF as transcriptional co-regulators of neuronal differentiation.

Network propagation connects TWIST1 with epigenetic regulators CHD7, CHD8, and WHSC1, which collectively promote the bias toward neural crest while suppressing neural stem cell programmes, and subsequently enhance ectomesenchyme potential.

Analysis of epigenome maps from human pancreatic progenitors and functional validation in zebrafish identify LAMA1 and CRB2 as type 2 diabetes risk-associated genes with roles in pancreatic development.

The short-lived tammar wallaby placenta expresses genes resembling eutherian placentas, establishing marsupials as "placental mammals", further, dynamic lactation allows marsupials to compensate for short placentation by expressing key placental genes in the mammary gland.

Investigation of how cells rewire their transcriptional programs during transition from mitotic to meiotic cell fate reveals a two-pronged mechanism for inactivating a key mitotic transcription factor.

Allele-specific expression, natural antisense transcripts, and developmental gene expression, but not RNA editing or developmental hourglass, act in concert to shape the transcriptome during the fruiting body formation of complex multicellular fungi.

The C terminal fusion partners of TAZ-CAMTA1, YAP-TFE3 and potentially other TAZ/YAP fusion proteins in cancer recruit epigenetic modifiers that modulate a baseline TEAD-based transcriptional program.

CD4+ T cells responding to chronic lymphocytic choriomeningitis virus infection display transcriptional heterogeneity that is marked by both lineage-specific gene expression profiles and core gene expression programs that are upregulated and conserved across multiple distinct populations of T helper cells.

Single-cell analyses of cells infected by Herpes Simplex Virus 1 revealed extreme heterogeneity among infected cells, including the robust activation of developmental gene programs in highly infected cells.