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Biology subjects

Jamal, A.

Publications and source records attributed to Jamal, A..

3 recordsLinked to original sources

Connectomic mapping of pharyngeal and gut sensory circuits in adult Drosophila

Feeding is regulated by both external sensory signals, such as taste, and internal sensory signals originating from the pharynx and gut. The recent completion of the Full Adult Fly Brain (FAFB) connectome offers an opportunity to map these sensory inputs and their downstream circuits. While the external gustatory receptor neurons have been relatively well characterized, the internal pharyngeal and gut sensory neurons remain less understood. Here, we systemically identify their axonal projections in the FAFB connectome and examine their downstream circuits. We find that the stomodeal nerve, which carries afferent signals from the gastrointestinal tract to the brain, contains multiple types of sensory axons with distinct morphology and downstream output connections. In addition, we identify sensory axons derived from different pharyngeal sense organs and find that chemosensory and mechanosensory axons arborize in distinct regions of the subesophageal zone. Characterization of the second-and third-order neurons reveals the major brain regions that receive input from pharyngeal and gut sensory neurons. Interestingly, a subset of these internal sensory neurons forms monosynaptic connections with various motor neurons and endocrine cells, suggesting that internal signals from the pharynx and gut may directly influence feeding-related motor programs and endocrine output. Together, our study delineates the pharyngeal and gut sensory circuits, laying a foundation for future studies on how internal sensory signals regulate feeding behavior and endocrine functions.

neuroscience↗

Impact of Parental Time-Restricted Feeding on Offspring Metabolic Phenotypic Traits

A substantial body of research elucidates the mechanisms and health advantages associated with intermittent fasting (IF). However, the impact of parental IF on offspring remains unclear. Through an investigation involving four IF and ad libitum combinations of parental mating groups, we demonstrate that parental IF (daily time-restricted feeding) influences offsprings metabolic health indicators in male and female offspring in distinct ways. We found that when both parents are on IF their offspring exhibit protection against the adverse effects of a high-fat, high-sugar, and high-salt diet in a sex-specific manner. This study underscores the potential significance of parental lifestyle modifications involving dietary restriction for the metabolic status of their children and their risk for obesity and diabetes.

genetics↗

Myofibroblast Ccn3 is regulated by Yap and Wwtr1 and contributes to adverse cardiac outcomes

While Yap and Wwtr1 regulate resident cardiac fibroblast to myofibroblast differentiation following cardiac injury, their role specifically in activated myofibroblasts remains unexplored. Here we assess the pathophysiological and cellular consequence of genetic depletion of Yap alone (Yapfl/fl;PostnMCM) or Yap and Wwtr1 (Yapfl/fl;Wwtr1fl/+;PostnMCM) in adult mouse myofibroblasts following myocardial infarction and identify and validate novel downstream factors specifically in cardiac myofibroblasts that mediate pathological remodeling. Following myocardial infarction, depletion of Yap in myofibroblasts had minimal effect on heart function while depletion of Yap/Wwtr1 resulted in smaller scars, reduced interstitial fibrosis, and improved ejection fraction and fractional shortening. Single cell RNA sequencing of interstitial cardiac cells 7 days post infarction showed suppression of pro-fibrotic genes in fibroblasts derived from Yapfl/fl,Wwtr1fl/+;PostnMCM hearts. In vivo myofibroblast depletion of Yap/Wwtr1 as well in vitro knockdown of Yap/Wwtr1 dramatically decreased RNA and protein expression of the matricellular factor Ccn3. Administration of recombinant CCN3 to adult mice following myocardial infarction remarkably aggravated cardiac function and scarring. CCN3 administration drove myocardial gene expression of pro-fibrotic genes in infarcted left ventricles implicating CCN3 as a novel driver of cardiac fibrotic processes following myocardial infarction.

physiology↗