We examined lifetime clutch production and size at maturity for blue crabs Callinectes sapidus Rathbun in North Carolina, USA. Female crabs were collected at terminal molt and confined individually in the field for the duration of their lifetime. Crabs were monitored weekly for the presence of eggs. Clutch quality and larval viability were assessed for each clutch. Crabs produced up to 7 clutches over 1 to 2 spawning seasons and survived up to 394 d after the terminal molt. Time to first clutch and time between clutches were positively correlated with carapace width and best described by degree-days, physiological time calculated as a thermal integral. Size at maturity was negatively correlated with water temperature on the day of the terminal molt. Egg lipid content (mean = 79.2% of dry mass), egg diameter (mean = 267.5 µm), larval carapace width (mean = 278.4 µm), and larval survival time without food (mean = 3.4 d) were similar for all clutches. The percentage of embryos developing normally decreased 40% from Clutch 1 to 4, and clutch volume decreased 50% from Clutch 1 to 5. Thus, most of a crab's reproductive output is from the first few clutches. Realistic estimates of fecundity and reproductive potential are essential for accurate spawning stock assessment and population modeling. KEY WORDS: Blue crab · Callinectes sapidus · Reproductive potential · Spawning biology · Fecundity · Multiple clutches · Degree-days Resale or republication not permitted without written consent of the publisherMar Ecol Prog Ser 394: [153][154][155][156][157][158][159][160][161][162][163] 2009 serves to reduce the risk of predation and sperm competition (Jivoff 1997). Thus, the duration of the postcopulatory embrace depends on the presence of conspecific predators, sex ratio, and male size and density (Jivoff 1997). Approximately 12% of females mate with at least a second male (Jivoff 1997). Females mate only following the terminal molt (Van Engel 1958); thus, all clutches produced by a female must be fertilized by stored sperm. Sufficient sperm is stored to fertilize up to a dozen clutches of eggs . Wolcott et al. (2005) found that the number and viability of sperm transferred during mating are independent of male and female body size. Female crabs then forage, develop mature ovaries, extrude a first clutch, and undertake a seaward spawning migration (Van Engel 1958, Tankersley et al. 1998, Turner et al. 2003, Forward et al. 2005) using both ebb-tide transport and directed walking during flood tides (Forward et al. 2003. Spawning females produce multiple clutches, and migratory behavior continues between clutches, ensuring that spawning females are continually moving seaward throughout the spawning season , Forward et al. 2005.Studies of crab and lobster reproductive potential have traditionally examined fecundity for only a single clutch (e.g. Pillay & Nair 1971, Hines 1982, Campbell & Robinson 1983, Jones & Simons 1983, Dugan et al. 1994, Medina Mantelatto & Fransozo 1997, presumably due to the difficulty of obser...
Chronic inflammation is a common feature of obesity with elevated cytokines such as Interleukin-1 (IL-1) in circulation and tissues. Here, we report an unconventional IL-1R-MyD88-IRAK2-PHB/OPA1 signaling axis that reprograms mitochondrial metabolism in adipocytes to exacerbate obesity. IL-1 induced recruitment of IRAK2-Myddosome to mitochondria outer membrane via recognition by TOM20, followed by TIMM50-guided translocation of IRAK2 into mitochondria inner membrane to suppress oxidative phosphorylation and fatty acid oxidation, thereby, attenuating energy expenditure. Adipocyte-specific MyD88 or IRAK2 deficiency reduced high fat diet (HFD)-induced weight gain, increased energy expenditure and ameliorated insulin resistance, associated with a smaller adipocyte size and increased cristae formation. IRAK2 kinase inactivation also reduced HFD-induced metabolic diseases. Mechanistically, IRAK2 suppressed respiratory super-complex formation via interaction with PHB1 and OPA1 upon stimulation of IL-1. Taken together, our results suggest that IRAK2 Myddosome functions as a critical link between inflammation and metabolism, representing a novel therapeutic target for patients with obesity.
ObjectiveBreakthroughs in HIV treatment, especially combination antiretroviral therapy (ART), have massively reduced AIDS-associated mortality. However, ART administration amplifies the risk of non-AIDS defining illnesses including obesity, diabetes, and cardiovascular disease, collectively known as metabolic syndrome. Initial reports suggest that ART-associated risk of metabolic syndrome correlates with socioeconomic status, a multifaceted finding that encompasses income, race, education, and diet. Therefore, determination of causal relationships is extremely challenging due to the complex interplay between viral infection, ART, and the many environmental factors.MethodsIn the current study, we employed a mouse model to specifically examine interactions between ART and diet that impacts energy balance and glucose metabolism. Previous studies have shown that high-fat feeding induces persistent low-grade systemic and adipose tissue inflammation contributing to insulin resistance and metabolic dysregulation via adipose-infiltrating macrophages. Studies herein test the hypothesis that ART potentiates the inflammatory effects of a high-fat diet (HFD). C57Bl/6J mice on a HFD or standard chow containing ART or vehicle, were subjected to functional metabolic testing, RNA-sequencing of epididymal white adipose tissue (eWAT), and array-based kinomic analysis of eWAT-infiltrating macrophages.ResultsART-treated mice on a HFD displayed increased fat mass accumulation, impaired glucose tolerance, and potentiated insulin resistance. Gene set enrichment and kinomic array analyses revealed a pro-inflammatory transcriptional signature depicting granulocyte migration and activation.ConclusionThe current study reveals a HFD-ART interaction that increases inflammatory transcriptional pathways and impairs glucose metabolism, energy balance, and metabolic dysfunction.
Reactive oxygen species (ROS) are commonly produced by algal, vascular plant, and animal cells involved in the innate immune response as cellular signals promoting defense and healing and/or as a direct defense against invading pathogens. The production of reactive species in macroalgae upon injury, however, is largely uncharacterized. In this study, we surveyed 13 species of macroalgae from the Western Antarctic Peninsula and show that the release of strong oxidants is common after macroalgal wounding. Most species released strong oxidants within 1 min of wounding and/or showed cellular accumulation of strong oxidants over an hour post-wounding. Exogenous catalase was used to show that hydrogen peroxide was a component of immediate oxidant release in one of five species, but was not responsible for the entire oxidative wound response as is common in vascular plants. The other component(s) of the oxidant cocktail released upon wounding are unknown. We were unable to detect protein nitration in extracts of four oxidant-producing species flash frozen 30 s after wounding, but a role for reactive nitrogen species such as peroxynitrite cannot be completely ruled out. Two species showed evidence for the production of a catalase-activated oxidant, a mechanism previously known only from the laboratory and from the synthetic drug isoniazid used to kill the human pathogen Mycobacterium tuberculosis. The rhodophyte Palmaria decipiens, which released strong oxidants after wounding, also produced strong oxidants upon grazing by a sympatric amphipod, suggesting that oxidants are involved in the response to grazing.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.