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"Ward, Chris"
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Genetic and phenotypic diversity of wine-associated Hanseniaspora species
Abstract
The genus Hanseniaspora includes apiculate yeasts commonly found in fruit- and fermentation-associated environments. Their genetic diversity and evolutionary adaptations remain largely unexplored despite their ecological and oenological significance. This study investigated the phylogenetic relationships, genome structure, selection patterns, and phenotypic diversity of Hanseniaspora species isolated primarily from Australian wine environments, focusing on Hanseniaspora uvarum, the most abundant non-Saccharomyces yeast in wine fermentation. A total of 151 isolates were sequenced, including long-read genomes for representatives of the main phylogenetic clades. Comparative genomics revealed ancestral chromosomal rearrangements between the slow-evolving lineage (SEL) and fast-evolving lineage (FEL) that could have contributed to their evolutionary split, as well as significant loss of genes associated with mRNA splicing, chromatid segregation and signal recognition particle protein targeting in the FEL. Pangenome analysis within H. uvarum identified extensive copy number variation, particularly in genes related to xenobiotic tolerance and nutrient transport. Investigation into the selective landscape following the FEL/SEL divergence identified diversifying selection in 229 genes in the FEL, with significant enrichment in genes within the lysine biosynthetic pathway. Furthermore, phenotypic screening of 116 isolates revealed substantial intraspecific diversity, with specific species exhibiting enhanced ethanol, osmotic, copper, SO₂, and cold tolerance.
This study provides novel insights into the genomic evolution and functional diversity of Hanseniaspora, expanding our understanding of yeast adaptation to wine fermentation and laying the foundation for targeted gene investigations within this important genus.
Journal Article
Land, liberation and compromise in Southern Africa
\"This book offers an analysis of the origins of the crisis in Zimbabwe and why it has had such a profound impact on both the land issue and democratic politics in the Southern African region. The analysis contributes to the present debates around Mugabe, neo-imperialism and the stability in the region\"--Provided by publisher.
Book
Recombination, admixture and genome instability shape the genomic landscape of Saccharomyces cerevisiae derived from spontaneous grape ferments
Cultural exchange of fermentation techniques has driven the spread of Saccharomyces cerevisiae across the globe, establishing natural populations in many countries. Despite this, Oceania is thought to lack native populations of S . cerevisiae , only being introduced after colonisation. Here we investigate the genomic landscape of 411 S . cerevisiae isolated from spontaneous grape fermentations in Australia across multiple locations, years, and grape cultivars. Spontaneous fermentations contained highly recombined mosaic strains that exhibited high levels of genome instability. Assigning genomic windows to putative ancestral origin revealed that few closely related starter lineages have come to dominate the genetic landscape, contributing most of the genetic variation. Fine-scale phylogenetic analysis of loci not observed in strains of commercial wine origin identified widespread admixture with European derived beer yeast along with three independent admixture events from potentially endemic Oceanic lineages that was associated with genome instability. Finally, we investigated Australian ecological niches for basal isolates, identifying phylogenetically distinct S . cerevisiae of non-European, non-domesticated origin associated with admixture loci. Our results illustrate the effect commercial use of microbes may have on local microorganism genetic diversity and demonstrates the presence of non-domesticated, potentially endemic lineages of S . cerevisiae in Australian niches that are actively admixing.
Journal Article
Novel attachment methods for assessing activity patterns using triaxial accelerometers on stingrays in the Bahamas
The use of bio-logging devices is important for describing behaviour, energy expenditure and activity budgets of cryptic marine organisms. In stingrays, the physical deployment of bio-logging devices is challenging due to their lack of raised structures or hard tissue for attachment. Previous studies have used a range of attachment techniques on various locations, including the pectoral musculature of the discs, spiracular cartilage or tail musculature. For devices such as accelerometers that capture precise animal movement, appropriate attachment and retention are important for collecting data that are representative of animal movement. Here, we detail a novel attachment method for bio-logging devices on stingrays using triaxial accelerometers that were attached through the musculature at the base of the tail of ten wild southern stingrays (Hypanus americanus). Data returned upon recapture suggest that stingrays exhibited active and non-active states and had the highest activity levels (vector sum acceleration) during the night with no apparent tide-associated activity patterns. Tag retention was 100% for all recaptured individuals (n = 8), with deployments lasting from 13 to 212 days. Wounds associated with the tagging process were completely healed for individuals that were recaptured after tag removal (n = 3). High rates of tag retention, usability and ecological significance of retrieved data, and complete healing following tag removal suggest that the methods described herein should be considered when attaching small bio-logging devices to large demersal rays for short- (weeks)-to-medium-term (months) studies.
Journal Article
Abnormal M1/M2 macrophage phenotype profiles in the small airway wall and lumen in smokers and chronic obstructive pulmonary disease (COPD)
We explore potential dysregulation of macrophage phenotypes in COPD pathogenesis through integrated study of human small airway tissue, bronchoalveolar lavage (BAL) and an experimental murine model of COPD. We evaluated human airway tissue and BAL from healthy controls, normal lung function smokers (NLFS), and COPD subjects. Both small airways and BAL cells were immunohistochemically stained with anti-CD68 for total macrophages and with anti-CD163 for M2, and anti-iNOS for M1 macrophages. Multiplex ELISA measured BAL cytokines. Comparable cigarette smoke-induced experimental COPD mouse model was assessed for relevant mRNA profiles. We found an increase in pro-inflammatory M1s in the small airways of NLFS and COPD compared to controls with a reciprocal decrease in M2 macrophages, which remained unchanged among pathological groups. However, luminal macrophages showed a dominant M2 phenotype in both NLFS and COPD subjects. BAL cytokine skewed towards an M2 profile with increase in CCL22, IL-4, IL-13, and IL-10 in both NLFS and COPDs. The mouse-model of COPD showed similar increase in mRNA for M2 markers. Our finding suggests abnormal macrophage switching in both mucosal and luminal areas of COPD patients, that strongly associated with cytokine balance. There may be potential for beneficial therapeutic cytokine manipulation of macrophage phenotypes in COPD.
Journal Article
Importance of epithelial mesenchymal transition (EMT) in COPD and asthma
Epithelial stimulation can also lead to malignancy, through type 3 EMT, that is, EMT plus angiogenesis, which we have documented in large airway. 3 The major criteria for recognising EMT activity in vivo were suggested by Zeisberg et al, 3 which emphasised especially reticular basement membrane (Rbm) fragmentation, due to transitioning epithelial cells digesting their way through to the lamina propria (LP), accompanied by expression of mesenchymal markers.
Journal Article
Circulating TNF-like protein 1A (TL1A) is elevated early in rheumatoid arthritis and depends on TNF
Background
The tumor necrosis factor (TNF) superfamily cytokine TNF-like protein 1A (TL1A) and its receptor DR3 are essential for diverse animal models of autoimmune disease and may be pathogenic in rheumatoid arthritis (RA). However, the relationship of TL1A to disease duration, activity, and response to anti-TNF and other therapies in RA is not clear.
Methods
We measured soluble TL1A in synovial fluid (SF), serum, or plasma from RA first-degree relatives (FDRs) and in early RA and established disease. We measured the effects of anti-TNF and methotrexate (MTX) therapy on circulating TL1A from multiple independent RA treatment trials. We also determined the ability of a blocking anti-TL1A antibody to inhibit clinical disease and articular bone destruction in the murine collagen-induced arthritis (CIA) model of human RA.
Results
Soluble TL1A was specifically elevated in the blood and SF of patients with RA compared to patients with other diseases and was elevated early in disease and in at-risk anti-cyclic citrullinated peptide (CCP) (+) first-degree relatives (FDRs). Therapeutic TNF inhibition reduced serum TL1A in both responders and non-responders, whereas TL1A declined following MTX treatment only in responders. In murine CIA, TL1A blockade was clinically efficacious and reduced bone erosions.
Conclusions
TL1A is specifically elevated in RA from early in the disease course and in at-risk FDRs. The decline in TL1A after TNF blockade suggests that TL1A levels may be a useful biomarker for TNF activity in RA. These results support the further investigation of the relationship between TL1A and TNF and TL1A blockade as a potential therapeutic strategy in RA.
Journal Article
Leaky Ca2+ release channel/ryanodine receptor 2 causes seizures and sudden cardiac death in mice
The Ca2+ release channel ryanodine receptor 2 (RyR2) is required for excitation-contraction coupling in the heart and is also present in the brain. Mutations in RyR2 have been linked to exercise-induced sudden cardiac death (catecholaminergic polymorphic ventricular tachycardia [CPVT]). CPVT-associated RyR2 mutations result in \"leaky\" RyR2 channels due to the decreased binding of the calstabin2 (FKBP12.6) subunit, which stabilizes the closed state of the channel. We found that mice heterozygous for the R2474S mutation in Ryr2 (Ryr2-R2474S mice) exhibited spontaneous generalized tonic-clonic seizures (which occurred in the absence of cardiac arrhythmias), exercise-induced ventricular arrhythmias, and sudden cardiac death. Treatment with a novel RyR2-specific compound (S107) that enhances the binding of calstabin2 to the mutant Ryr2-R2474S channel inhibited the channel leak and prevented cardiac arrhythmias and raised the seizure threshold. Thus, CPVT-associated mutant leaky Ryr2-R2474S channels in the brain can cause seizures in mice, independent of cardiac arrhythmias. Based on these data, we propose that CPVT is a combined neurocardiac disorder in which leaky RyR2 channels in the brain cause epilepsy, and the same leaky channels in the heart cause exercise-induced sudden cardiac death.
Journal Article
The Underappreciated Role of Epithelial Mesenchymal Transition in Chronic Obstructive Pulmonary Disease and Its Strong Link to Lung Cancer
The World Health Organisation reported COPD to be the third leading cause of death globally in 2019, and in 2020, the most common cause of cancer death was lung cancer; when these linked conditions are added together they come near the top of the leading causes of mortality. The cell-biological program termed epithelial-to-mesenchymal transition (EMT) plays an important role in organ development, fibrosis and cancer progression. Over the past decade there has emerged a substantial literature that also links EMT specifically to the pathophysiology of chronic obstructive pulmonary disease (COPD) as primarily an airway fibrosis disease; COPD is a recognised strong independent risk factor for the development of lung cancer, over and above the risks associated with smoking. In this review, our primary focus is to highlight these linkages and alert both the COPD and lung cancer fields to these complex interactions. We emphasise the need for inter-disciplinary attention and research focused on the likely crucial roles of EMT (and potential for its inhibition) with recognition of its strategic place mechanistically in both COPD and lung cancer. As part of this we discuss the future potential directions for novel therapeutic opportunities, including evidence-based strategic repurposing of currently used familiar/approved medications.
Journal Article