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MacLeod, K.

Publications and source records attributed to MacLeod, K..

3 recordsLinked to original sources

Winter warming shapes gut microbiome composition and directional dysbiosis in a temperate lizard

Environmental temperature shapes ectotherm gut microbiomes through direct effects on community structure and indirect effects mediated by host physiology. Due to climate change, winter temperatures are rising, in some regions faster than summer temperatures. However, warming effects on the microbiome during overwintering remain poorly understood compared to the active season, limiting predictions of host-microbiome responses across the annual cycle. We experimentally tested how winter warming influences gut microbiome diversity and composition in the common wall lizard (Podarcis muralis). Thirty-nine lizards were overwintered under cold (4{+/-}1{degrees}C), mild (8{+/-}1{degrees}C), or fluctuating (5 days cold, 2 days mild) temperatures, and 80 faecal samples were collected post-emergence for 16S rRNA gene sequencing. Winter warming did not alter alpha diversity but induced consistent shifts in community composition relative to the cold treatment, with distinct responses to constant versus fluctuating warming. Constant mild temperatures enriched fewer taxa, including putatively opportunistic or pathogenic genera, potentially signalling microbiome imbalance. In contrast, fluctuating warming and the baseline cold treatment preserved a broader suite of fermentative bacteria, likely supporting more stable gut homeostasis. Both warming treatments increased directional dysbiosis relative to the cold treatment, though without increasing interindividual variability, indicating structured reassembly rather than stochastic change. Our findings suggest that winter warming can subtly negatively affect gut microbiomes and host health, while fluctuating temperatures may buffer negative effects. We show that overwintering is an important, yet overlooked, period through which climate warming can shape host-microbiome dynamics.

ecology↗

The ORGAN SIZE (ORG) locus contributes to isometric gigantism in domesticated tomato

Gigantism is a key component of the domestication syndrome, a suite of traits that differentiates crops from their wild relatives. Allometric gigantism is strongly marked in horticultural crops, causing disproportionate increases in the size of edible parts such as stems, leaves or fruits. Tomato (Solanum lycopersicum) has attracted attention as a model for fruit gigantism, and many genes have been described controlling this trait. However, the genetic basis of a corresponding increase in size of vegetative organs contributing to isometric gigantism, has remained relatively unexplored. Here, we identified a 0.4 Mbp region on chromosome 7 in introgression lines (ILs) from the wild species Solanum pennellii in two different tomato genetic backgrounds (cv. M82 and cv. Micro-Tom) that controls vegetative and reproductive organ size in tomato. The locus, named ORGAN SIZE (ORG), was fine-mapped using genotype-by-sequencing. A survey of literature revealed that ORG overlaps with previously mapped QTLs controlling tomato fruit weight during domestication. Alleles from the wild species led to reduced cell number in different organs, which was partially compensated by greater cell expansion in leaves but not in fruits. The result was a proportional reduction in leaf, flower and fruit size in the ILs harbouring the wild alleles. These findings suggest that selection for large fruit during domestication also tends to select for increases in leaf size by influencing cell division. Since leaf size is relevant for both source-sink balance and crop adaptation to different environments, the discovery of ORG could allow fine-tuning of these parameters. One sentence summaryA locus that controls isometric size increase in vegetative and reproductive organs of tomato through changes in cell division

plant biology↗

Pathogenic potential of Hic1 expressing cardiac stromal progenitors

The cardiac stroma contains multipotent mesenchymal progenitors. However, lineage relationships within cardiac stromal cells are still poorly understood. Here, we identify heart-resident PDGFRa+ Sca-1+ cells as cardiac Fibro/Adipogenic Progenitors (cFAPs) and show that they respond to ischemic damage by generating fibrogenic cells. Pharmacological blockade of this differentiation step with an anti-fibrotic tyrosine kinase inhibitor decreases post-myocardial infarction (MI) remodeling and leads to improvements in heart function. In the undamaged heart, activation of cFAPs through lineage-specific deletion of the quiescence factor Hic1 reveals additional pathogenic potential, causing fibro-fatty infiltration of the myocardium and driving major pathological features of Arrhythmogenic Cardiomyopathy (AC). HighlightsO_LIA subpopulation of PDGFRa+, Sca-1+ cells, previously considered to be a sub-type of cardiac fibroblasts, are multipotent mesenchymal progenitors, C_LIO_LICardiac damage triggers the differentiation of PDGFRa+ Sca-1+ cells into Sca-1- cells expressing a fibrogenic transcriptional programme, C_LIO_LIBlockade of the cFAP-to-fibroblast transition by Nilotinib ameliorated cardiac dysfunction post-MI and modulated cardiac remodelling. C_LIO_LIStudies performed on a model of experimentally-induced AC confirmed that cFAPs are a source of both cardiac fibroblasts and adipocytes in vivo. C_LIO_LIConversely, in the undamaged heart, activation of cFAPs by means of lineage-specific deletion of transcription factor Hic1, resulted in fibro/fatty cardiac degeneration and pathological alterations reminiscent of AC. Collectively, our findings show that a proportion of what are commonly termed "fibroblasts" are actually multipotent mesenchymal progenitors that contribute to different forms of cardiac degeneration depending on the damage setting. C_LI

cell biology↗