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Martin, L. E.

Publications and source records attributed to Martin, L. E..

3 recordsLinked to original sources

Warmer temperature accelerates senescence by modifying the aging-dependent changes in the mosquito transcriptome, altering immunity, metabolism, and DNA repair

BackgroundGlobal environmental temperatures are rising, which is increasing the body temperature of mosquitoes. This increase in body temperature is accelerating senescence, thereby weakening immune responses and reproductive processes, and shortening lifespan. To determine how warmer temperature and aging, individually and interactively, shape the transcriptome of the African malaria mosquito, Anopheles gambiae, we conducted RNA-sequencing and network-analysis in naive and immune-induced mosquitoes that had been reared at 27C, 30C or 32C and were 1, 5, 10 or 15 days into adulthood. Results: We demonstrate that immune induction, warmer temperature, and aging alter the transcriptome. Notably, the transcriptome of 1-day-old mosquitoes is pronouncedly different from older mosquitoes, and importantly, warmer temperature modifies the aging-dependent changes to accelerate senescence. For example, warmer temperature amplifies the aging-dependent decrease in immune gene expression but dampens both the aging-dependent decrease in metabolic gene expression and the aging-dependent increase in DNA repair gene expression. ConclusionsAltogether, warmer temperature accelerates senescence, shaping the transcriptome in ways that alter the mosquitos ability to fight infection and survive in a warming environment.

zoology↗

Multiple PLCβ signaling pathways in taste receptor cells contribute to the detection of bitter, sweet and umami stimuli

Taste receptor cells use multiple signaling pathways to detect chemicals in potential food items. These cells are functionally grouped into different types: Type I cells act as support cells and have glial-like properties; Type II cells detect bitter, sweet, and umami taste stimuli; and Type III cells detect sour and salty stimuli. We have identified a new population of taste cells that are broadly tuned to multiple taste stimuli including bitter, sweet, sour and umami. The goal of this study was to characterize these broadly responsive (BR) taste cells. We used an IP3R3-KO mouse (does not release calcium (Ca2+) from Type II cells when stimulated with bitter, sweet or umami stimuli) to characterize the BR cells without any potentially confounding input from Type II cells. Using live cell Ca2+ imaging in isolated taste cells from the IP3R3-KO mouse, we found that BR cells are a subset of Type III cells that respond to sour stimuli but also use a PLC{beta}3 signaling pathway to respond to bitter, sweet and umami stimuli. Unlike Type II cells, individual BR cells are broadly tuned and respond to multiple stimuli across different taste modalities. Live cell imaging in a PLC{beta}3-KO mouse confirmed that BR cells use a PLC{beta}3 signaling pathway to generate Ca2+ signals to bitter, sweet and umami stimuli. Analysis of c-Fos activity in the nucleus of the solitary tract (NTS) and short term behavioral assays revealed that BR cells make significant contributions to taste.

neuroscience↗

Differential effects of diet and weight on taste responses in diet-induced obese mice

The ever growing obesity epidemic has created a need to develop a better understanding of the underlying mechanisms responsible for this condition. Appetite and consumption are directly influenced by the taste system which determines if potential food items will be ingested or rejected. While previous studies have reported that obese individuals have reduced taste perception, the relationship between these processes is still poorly understood. Earlier work has demonstrated that diet-induced obesity (DIO) directly impairs taste responses, particularly for sweet stimuli. These deficits occurred in the cells located in the oral cavity as well as in the behavioral responses. However, it is not clear if these changes to the taste system are due to obesity or to the high fat diet exposure. The goal of the current study was to determine if diet or excess weight is responsible for the DIO induced taste deficits. Using a combination of live cell imaging, brief-access licking, immunohistochemistry and real-time PCR, we have found that diet and weight gain can each selectivity affect taste. Follow up experiments determined that two key signaling proteins, gustducin and phospholipase C{beta}2, are significantly reduced in the high fat diet without weight gain and obese mice, identifying a potential mechanism for the reduced taste responsiveness to some stimuli. Our data indicate that the relationship between obesity and taste is complex and reveal that for some stimuli, diet alone can cause taste deficits, even without the onset of obesity.

neuroscience↗