Life cycle and development of the marine leech Branchellion lobata (Hirudinea: Piscicolidae), from round stingrays, Urobatis halleri, from southern California.

During captivity, round stingrays, Urobatis halleri, became infected with the marine leech Branchellion lobata. When adult leeches were deprived of blood meal, they experienced a rapid decrease in body mass and did not survive beyond 25 days. If kept in aquaria with host rays, B. lobata fed frequently and soon produced cocoons, which were discovered adhered to sand grains. A single leech emerged from each cocoon (at ~ 21 days), and was either preserved for histology or molecular analysis, or monitored for development by introduction to new hosts in aquaria. Over a 74-day observation period, leeches grew from ~ 2 to 8 mm without becoming mature. Newly hatched leeches differed from adults in lacking branchiae and apparent pulsatile vesicles. The microbiome of the hatchlings was dominated by a specific, but undescribed, member of the gammaproteobacteria, also recovered previously from the adult leech microbiome. Raising B. lobata in captivity provided an opportunity to examine their reproductive strategy and early developmental process, adding to our limited knowledge of this common group of parasites.

Trefoil Factor 2 Expressed by the Murine Pancreatic Acinar Cells Is Required for the Development of Islets and for ß-Cell Function During Aging.

Exocrine-to-endocrine cross talk in the pancreas is crucial to maintain ß-cell function. However, the molecular mechanisms underlying this cross talk are largely undefined. Trefoil factor 2 (Tff2) is a secreted factor known to promote the proliferation of ß-cells in vitro, but its physiological role in vivo in the pancreas is unknown. Also, it remains unclear which pancreatic cell type expresses Tff2 protein. We therefore created a mouse model with a conditional knockout of Tff2 in the murine pancreas. We find that the Tff2 protein is preferentially expressed in acinar but not ductal or endocrine cells. Tff2 deficiency in the pancreas reduces ß-cell mass on embryonic day 16.5. However, homozygous mutant mice are born without a reduction of ß-cells and with acinar Tff3 compensation by day 7. When mice are aged to 1 year, both male and female homozygous and male heterozygous mutants develop impaired glucose tolerance without affected insulin sensitivity. Perifusion analysis reveals that the second phase of glucose-stimulated insulin secretion from islets is reduced in aged homozygous mutant compared with controls. Collectively, these results demonstrate a previously unknown role of Tff2 as an exocrine acinar cell-derived protein required for maintaining functional endocrine ß-cells in mice.