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Biology subjects

Corcoran, E.

Publications and source records attributed to Corcoran, E..

3 recordsLinked to original sources

Better Safe Than Sorry: Leg Amputations as a Prophylactic Wound Care Behaviour in Carpenter Ants

Animals often sustain injuries, which are susceptible to lethal infections. In social insects, wound care behaviours have evolved to reduce these risks. But the limits of wound care behaviours remain unclear. Here we investigated the wound care behaviours of the ant Camponotus maculatus. Our findings show that amputation of legs infected with Pseudomonas aeruginosa significantly reduced mortality. However, nestmates do not differentiate between infected and sterile injuries, providing similar treatments regardless of infection. Even though we show that early amputation correlates with higher survival rates, nestmates amputate indiscriminately on legs with fresh or old wounds. Additionally, cuticular hydrocarbon profiles differed between ants with infected or sterile wounds only 24 hours post-injury, a timepoint when amputations are no longer effective. We propose that C. maculatus workers perform prophylactic amputations regardless of injury state or age. This is in sharp contrast to previous studies which showed clear capabilities to treat infected wounds differently in ants using antimicrobial compounds. This work therefore shows the limits of wound care behaviours in social insects, allowing us to better understand the evolutionary drivers of this unique behaviour.

animal behavior and cognition↗

N-Glycans on the extracellular domain of the Notch1 receptor control Jagged-1 induced Notch signalling and myogenic differentiation of S100β resident vascular stem cells

Notch signalling, critical for development and postnatal homeostasis of the vascular system, is highly regulated by several mechanisms including glycosylation. While the importance of O-linked glycosylation is widely accepted, the structure and function of N-glycans has yet to be defined. Here, we take advantage of lectin binding assays in combination with pharmacological, molecular, and site-directed mutagenetic approaches to study N-glycosylation of the Notch1 receptor. We find that several key oligosaccharides containing bisecting or core fucosylated structures decorate the receptor, control expression and receptor trafficking, and dictate Jagged-1 activation of Notch target genes and myogenic differentiation of multipotent S100{beta} vascular stem cells. N-glycans at asparagine (N) 1241 and 1587 protect the receptor from accelerated degradation, while the oligosaccharide at N888 directly affects signal transduction. Conversely, N-linked glycans at N959, N1179, N1489 do not impact canonical signalling but inhibit differentiation. Our work highlights a novel functional role for N-glycans in controlling Notch1 signalling and differentiation of vascular stem cells. TeaserA sweet development in Notch regulation of vascular smooth muscle cell differentiation

cell biology↗

The calcium binding protein S100β marks Hedgehog-responsive perivascular stem cells that contribute to intimal thickening following iatrogenic flow restriction

A hallmark of subclinical atherosclerosis is the accumulation of vascular smooth muscle cell (SMC)-like cells leading to intimal thickening. While medial SMCs contribute, the participation of hedgehog responsive resident vascular stem cells (vSCs) to lesion formation remains unclear. Using transgenic eGFP mice and genetic lineage tracing of S100{beta} vSCs in vivo, we identified S100{beta}/Sca1 cells derived from a S100{beta} non-SMC parent population within lesions that co-localise with smooth muscle -actin (SMA) cells following iatrogenic flow restriction, an effect attenuated following hedgehog inhibition with the smoothened inhibitor, cyclopamine. In vitro, S100{beta}/Sca1 cells isolated from atheroprone regions of the mouse aorta expressed hedgehog signalling components, acquired the di-methylation of histone 3 lysine 4 (H3K4me2) stable SMC epigenetic mark at the Myh11 locus and underwent myogenic differentiation in response to recombinant sonic hedgehog (SHh). Both S100{beta} and PTCH1 cells were present in human vessels while S100{beta} cells were enriched in arteriosclerotic lesions. Recombinant SHh promoted myogenic differentiation of human induced pluripotent stem cell-derived S100{beta} neuroectoderm progenitors In vitro. We conclude that hedgehog responsive S100{beta} vSCs contribute to lesion formation and support targeting hedgehog signalling to treat subclinical arteriosclerosis.

cell biology↗