Key to the success of intracellular pathogens is the ability to sense and respond to a changing host cell environment. Macrophages exposed to microbial products undergo metabolic changes that drive inflammatory responses. However, the role of macrophage metabolic reprogramming in bacterial adaptation to the intracellular environment has not been explored. Here, using metabolic profiling and dual RNA sequencing, we show that succinate accumulation in macrophages is sensed by intracellular Salmonella Typhimurium (S. Tm) to promote antimicrobial resistance and type III secretion. S. Tm lacking the succinate uptake transporter DcuB displays impaired survival in macrophages and in mice. Thus, S. Tm co-opts the metabolic reprogramming of infected macrophages as a signal that induces its own virulence and survival, providing an additional perspective on metabolic host–pathogen cross-talk.

Article Virus-Induced Changes in mRNA Secondary Structure Uncover cis-Regulatory Elements that Directly Control Gene Expression Graphical Abstract Highlights d Mapping dynamic RNA structures provides a strategy to identify regulatory regions d Translation plays a major role in unwinding secondary structures in vivo d Structurally dynamic 3 0 UTRs are enriched in elements that regulate mRNA stability d CDS regions contain dynamic structural elements that regulate translation

Background: Polyamines are required for the process of adipogenesis. Results: Polyamine depletion causes inactivation of C/EBP␤ that is correlated with elevation of CHOP, and independently causes inhibition of mitotic clonal expansion. Conclusion: Polyamines are required for both main hubs of adipogenesis; completion of MCE and activation of C/EBP␤. Significance: Our results assist clarifying the mechanism by which polyamines support adipogenesis.

The Ten-a gene of Drosophila melanogaster encodes several alternative variants of a full length member of the Odz/Tenm protein family. A number of Ten-a mutants created by inexact excisions of a resident P-element insertion are embryonic lethal, but show no pair-rule phenotype. In contrast, these mutants, and deficiencies removing Ten-a, do enhance the segmentation phenotype of a weak allele of the paralog gene odz (or Ten-m) to the odz amorphic phenotype. Germ line clone derived Ten-a(-) embryos display a pair-rule phenotype which phenocopies that of odz. Post segmentation eye patterning phenotypes of Ten-a mutants establish it as a pleiotropic patterning co-partner of odz.

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