Vitamin D is not required for adaptive immunity to listeria.

Although ex vivo research suggests that vitamin D may play a role in innate and adaptive immunity, clear in vivo evidence is lacking. We have tested whether severe vitamin D deficiency alters the ability of mice to resist infection by Listeria. Our results show that vitamin D deficiency does not affect the LD50 of naïve mice in response to Listeria. To study the adaptive immune response, the LD50 for Listeria-immunized mice was determined for vitamin D-deficient and vitamin D-sufficient mice. Although the LD50 clearly increased by immunization with inactivated Listeria, there was no effect of vitamin D deficiency on survival of mice infected with wild-type Listeria. Thus, in this model of adaptive immunity, we could find no evidence of a role for vitamin D.

dsdA Does Not Affect Colonization of the Murine Urinary Tract by Escherichia coli CFT073.

The urinary tract environment provides many conditions that deter colonization by microorganisms. D-serine is thought to be one of these stressors and is present at high concentrations in urine. D-serine interferes with L-serine and pantothenate metabolism and is bacteriostatic to many species. Uropathogenic Escherichia coli commonly possess the dsdCXA genetic locus, which allows them to use D-serine as a sole carbon, nitrogen, and energy source. It was previously reported that in the model UPEC strain CFT073, a dsdA mutant outcompetes wild type in the murine model of urinary tract infection. This "hypercolonization" was used to propose a model whereby UPEC strains sense D-serine in the urinary tract and subsequently up-regulate genes necessary for pathogenesis. Here, we show that inactivation of dsdA does not lead to hypercolonization. We suggest that this previously observed effect is due to an unrecognized secondary mutation in rpoS and that some D-serine specific effects described in other studies may be affected by the rpoS status of the strains used. Inactivation of dsdA in the original clinical isolate of CFT073 gives CFT073 ΔdsdA a growth defect in human urine and renders it unable to grow on minimal medium containing D-serine as the sole carbon source. However, CFT073 ΔdsdA is able to colonize the urinary tracts of CBA/J mice indistinguishably from wild type. These findings indicate that D-serine catabolism, though it may play role(s) during urinary tract infection, does not affect the ability of uropathogenic E. coli to colonize the murine urinary tract.

Budding and braking news about clathrin-mediated endocytosis.

Clathrin-mediated endocytosis (CME) is the predominate mechanism of endocytosis in eukaryotes, but an understanding of this mechanism in plants has lagged behind yeast and mammalian systems. The generation of Arabidopsis mutant libraries, and the development of the molecular tools and equipment necessary to characterize these plant lines has led to an astonishing number of new insights into the mechanisms of membrane trafficking in plants. Over the past few years progress has been made on identifying, and in some instances confirming, the core components of CME in plants. This review focuses on the recent progress made in the understanding of the mechanism and regulation of CME in plants.