Biology subjects

Wrightson, K. L. C.

Publications and source records attributed to Wrightson, K. L. C..

2 recordsLinked to original sources

bioRxiv2024

Honey bee egg composition changes seasonally and after acute maternal virus infection

Honey bee (Apis mellifera) colonies depend on the reproductive output of their queens, which in turn is contingent on the care provided by worker bees. Viral infections in queens can compromise reproductive output, while worker infections can inhibit the successful functioning of a colony and its ability to care for the queen. Transgenerational immune priming (TGIP) occurs when queens transfer immune-related compounds or immune elicitors to their offspring, enhancing the ability of subsequent generations to resist infections. These maternal effects on offspring could positively impact colony health and resilience to viral infections, but little is currently known about TGIP for viruses. In this study, we investigate how viral infections affect the proteomic composition of eggs laid by virus-challenged queens (injected with a mixture of black queen cell virus and deformed wing virus B), both in controlled experimental settings and natural field conditions. Our results showed that virus-challenged queens upregulated immune effectors in their eggs and ovaries. In contrast, naturally infected queens from field surveys did not; there were no significant differences in egg protein, lipid, or metabolite composition related to maternal viral load or ovary size. However, egg collection date strongly influenced egg composition, likely reflecting seasonal variations in pollen resources. These findings highlight that while viral infections can induce transgenerational effects on egg proteomes under short-term experimental conditions, such effects are less apparent in natural settings and can be overshadowed by seasonal and other ecological factors.

zoology↗

bioRxiv2022

Deletion of carboxypeptidase E in beta cells disrupts proinsulin processing and alters beta cell identity in mice

Carboxypeptidase E (CPE) facilitates the conversion of prohormones into mature hormones and is highly expressed in multiple neuroendocrine tissues. Carriers of CPE mutations have elevated plasma proinsulin and develop severe obesity and hyperglycemia. We aimed to determine whether loss of Cpe in pancreatic beta cells disrupts proinsulin processing and accelerates development of diabetes and obesity in mice. Pancreatic beta cell-specific Cpe knockout mice ({beta}CpeKO; Cpefl/fl x Ins1Cre/+) lack mature insulin granules and have elevated proinsulin in plasma; however, glucose-and KCl-stimulated insulin secretion in {beta}CpeKO islets remained intact. High fat diet-fed {beta}CpeKO mice showed comparable weight gain and glucose tolerance compared to Wt littermates. Notably, beta-cell area was increased in chow-fed {beta}CpeKO mice and beta-cell replication was elevated in {beta}CpeKO islets. Transcriptomic analysis of {beta}CpeKO beta cells revealed elevated glycolysis and Hif1-target gene expression. Upon high glucose challenge, beta cells from {beta}CpeKO mice showed reduced mitochondrial membrane potential, increased reactive oxygen species, reduced MafA, and elevated Aldh1a3 transcript levels. Following multiple low-dose streptozotocin treatment, {beta}CpeKO mice had accelerated hyperglycemia with reduced beta-cell insulin and Glut2 expression. These findings suggest that Cpe and proper proinsulin processing are critical in maintaining beta cell function during the development of diabetes.

physiology↗