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PNAS Papers on Acute Kidney Injury, Parental Expression in Horse Placenta, Sea Urchin Microbes

Editor's Note: Some of the articles described below are not yet available at the PNAS site, but they are scheduled to be posted this week.

Investigators from Korea and Germany look at a fibroblast growth factor 23 (FGF23) pathway influencing acute kidney injury, following from past studies that linked enhanced FGF23 levels in the blood with increased acute kidney injury progression and mortality risk. Based on expression profiling and other experiments on a mouse model of acute kidney injury provoked by folic acid, the team detected a rise in expression by an orphan nuclear receptor called ERR-gamma in the liver, which appeared to coincide with hepatic FGF23 production. On the other hand, blood plasma levels of the FGF23 hormone were reduced when the authors dialed down ERR-gamma levels in the liver or using a drug agonist, prompting them to suggest that "hepatocytes are the major source of FGF23, and orphan nuclear receptor ERR-gamma is a novel transcriptional regulator of hepatic FGF23 production in [acute kidney injury]."

A team from the US, Belgium, Egypt, and Australia outlines examples of parental-specific allelic expression in horse placental samples. Using stranded RNA sequencing, paired-end RNA-seq, and whole-genome sequencing, the researchers profiled equine chorioallantois samples from the placenta as well as samples from each parent animal, identifying 1,336 genes showing apparent allele-specific expression. From there, they narrowed in more than 250 genes suspected of acting as imprinted genes — a set that was subsequently followed transcriptionally over the gestation process. "Our gene ontology analysis implies that maternally expressed genes tend to decrease the length of gestation, while paternally expressed genes extend the length of gestation," the authors report, adding that insights from the study "will provide the basis of better understanding the role of parental gene expression in the placenta during gestation."

Researchers from University of North Carolina at Charlotte, Vanderbilt University, and elsewhere describe a microbial community shifts in Heliocidaris sea urchins moving from feeding to non-feeding life history states. With the help of 16S ribosomal RNA gene sequencing, the team tracked bacterial communities in the feeding, "planktotrophic" sea urchin H. tuberculata and in the related, non-feeding "lecithotrophic" H. erythrogramma species, uncovering a dip in gut microbial diversity and wealth during lecithorophy as well as an apparent symbiotic role for Rickettsiales bacteria in H. erythrogramma. "Our results indicate that the evolutionary loss of a functional gut correlates with a reduction in the microbiome and the association with an endosymbiont," the authors write, suggesting "[s]ymbiotic transitions can therefore accompany life history transitions in the evolution of developmental strategies."

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