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Biology subjects

Gold, M.

Publications and source records attributed to Gold, M..

4 recordsLinked to original sources

Using gas exchange measurements to monitor growth, energy expenditure, and body composition of black soldier fly larvae (Hermetia illucens) on diets varying in protein-to-carbohydrate ratio

Optimizing black soldier fly larvae (BSFL) production requires a better understanding of how diet composition shapes growth, nutrient allocation, and metabolic efficiency. This study investigated whether respiratory measurements could serve as predictive, non-invasive tools for BSFL performance on diets differing in protein-to-carbohydrate (P:C) ratio. Larvae were reared for seven days on four experimental diets, with growth, survival, gas exchange (O2 consumption, CO2 production, respiratory exchange ratio (RER)), and body composition (crude protein and lipid contents) measured across seven replicates per treatment. O2 consumption correlated strongly with final larval biomass, while RER was closely associated with protein and lipid deposition. Larvae on low-protein, high-carbohydrate diets accumulated proportionally more lipid, whereas protein-rich diets increased crude protein content but required higher energetic investment. This demonstrates that lipid-rich larvae grew more efficient in energetic terms per unit accumulated biomass than protein-rich larvae. Across diets, gas exchange variables reliably reflected growth dynamics, metabolic activity, and nutrient assimilation. Integrating respirometry into rearing systems could enable real-time monitoring of insect biomass yield and nutrient composition.

physiology↗

An oligodendrocyte silencer element underlies the pathogenic impact of lamin B1 structural variants

The role of non-coding regulatory elements and how they might contribute to tissue type specificity of disease phenotypes is poorly understood. Autosomal Dominant Leukodystrophy (ADLD) is a fatal, adult-onset, neurological disorder that is characterized by extensive CNS demyelination. Most cases of ADLD are caused by tandem genomic duplications involving the lamin B1 gene (LMNB1) while a small subset are caused by genomic deletions upstream of the gene. Utilizing data from recently identified families that carry LMNB1 gene duplications but do not exhibit demyelination, ADLD patient tissues, CRISPR modified cell lines and mouse models, we have identified a novel silencer element that is lost in ADLD patients and that specifically targets overexpression to oligodendrocytes. This element consists of CTCF binding sites that mediate three-dimensional chromatin looping involving the LMNB1 and the recruitment of the PRC2 repressor complex. Loss of the silencer element in ADLD identifies a previously unknown role for silencer elements in tissue specificity and disease causation.

genetics↗

Human Lung-resident Mucosal-Associated Invariant T cells are Abundant, Express Antimicrobial Proteins, and are Cytokine Responsive

Mucosal-associated Invariant T (MAIT) cells are an innate-like T cell subset that recognize a broad array of microbial pathogens, including respiratory pathogens. Here we investigate the transcriptional profile of MAIT cells localized to the human lung, and postulate that MAIT cells may play a role in maintaining homeostasis at this mucosal barrier. Using the MR1/5-OP-RU tetramer, we identified MAIT cells and non-MAIT CD8+ T cells in lung tissue not suitable for transplant from human donors. We used RNA-sequencing of MAIT cells compared to non-MAIT CD8+ T cells to define the transcriptome of MAIT cells in the human lung. We show that, as a population, lung MAIT cells are polycytotoxic, secrete the directly antimicrobial molecule IL-26, express genes associated with persistence, and selectively express cytokine and chemokine-related molecules distinct from other lung-resident CD8+ T cells, such as interferon-{gamma}- and IL-12-receptors. These data highlight MAIT cells predisposition to rapid pro-inflammatory cytokine responsiveness and antimicrobial mechanisms in human lung tissue, concordant with findings of blood-derived counterparts, and support a function for MAIT cells as early sensors in the defense of respiratory barrier function.

immunology↗

AKAP79 enables calcineurin to directly suppress protein kinase A activity

Interplay between the second messengers cAMP and Ca2+ is a hallmark of dynamic cellular processes. A common motif is the opposition of the Ca2+-sensitive phosphatase calcineurin and the major cAMP receptor, protein kinase A (PKA). Calcineurin dephosphorylates sites primed by PKA to bring about changes including synaptic long-term depression (LTD). AKAP79 supports signaling of this type by anchoring PKA and calcineurin in tandem. In this study, we discovered that AKAP79 increases the rate of calcineurin dephosphorylation of type II PKA regulatory subunits by an order of magnitude. Fluorescent PKA activity reporter assays, supported by kinetic modeling, show how AKAP79-enhanced calcineurin activity enables suppression of PKA without altering cAMP levels by increasing PKA catalytic subunit capture rate. Experiments with hippocampal neurons indicate that this mechanism contributes towards LTD. This non- canonical mode of PKA regulation may underlie many other cellular processes.

biochemistry↗