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Bar, I.

Publications and source records attributed to Bar, I..

6 recordsLinked to original sources

Characterization of the molecular mechanisms of early sexual maturation stages in the Australian greenlip abalone (Haliotis laevigata)

Sexual maturation is a critical developmental transition in abalone, yet its molecular basis remains unclear. Understanding the mechanisms underlying maturation is essential for improving the yield and quality of aquaculture production. This study employed transcriptomic analysis to identify key genes involved in the early stages of sexual maturation in the greenlip abalone (Haliotis laevigata), a commercially and ecologically important species native to Australia. Among the most significantly differentially expressed genes were members of the 5-hydroxytryptamine receptor, cytochrome P450, and HSP70 families, which are associated with neuroendocrine signalling, steroid metabolism, and cellular stress response, respectively. Gene regulatory network analysis further predicted their upstream and downstream interactions, suggesting potential signalling pathways that may coordinate reproductive initiation. These findings provide new insights into the molecular mechanisms underlying early maturation in abalone and establish a foundation for future functional investigations.

genomics↗

Transcriptomic responses to Marteilia sydneyi infection in the Sydney rock oyster Saccostrea glomerata

Marteilia sydneyi, an ascetosporean parasite, is the causative agent of Queensland Unknown (QX) disease in Saccostrea glomerata. QX disease outbreaks often lead to high mortality rates and considerable population losses. Investigating host/parasite interactions at a molecular level is imperative to better understand how S. glomerata mounts immune defences, and to explore whether M. sydneyi evades host responses. This study aims to investigate S. glomeratas response to M. sydneyi infection through differential gene expression analysis to uncover immune mechanisms and potential markers for resistance. RNA sequencing and differential gene expression analysis revealed widespread transcriptional changes between infected and non-infected oysters. Genes encoding proteins involved in pathogen recognition and immune response signalling, such as galectin-4-like and G-protein coupled receptors, were significantly differentially expressed in S. glomerata infected with M. sydneyi, suggesting involvement in the hosts immune responses. Moreover, the upregulation of cytochrome P450 family genes indicate increases in the hosts detoxification processes and metabolic pathways, a possible response to infection-induced stress. However, extracellular superoxide dismutase, a gene previously implicated in the oxidative stress response to pathogens, was significantly downregulated, suggesting potential suppression of oxidative burst defence mechanisms. These results reveal the complex nature of S. glomeratas response to M. sydneyi infection, and possible suppression or evasion of host defences by the parasite. The study also identifies multiple genes that likely play crucial roles in the molecular responses and defence mechanisms of S. glomerata to M. sydneyi infection. The identification of these genes provides potential target genes for future studies and possible biomarkers for breeding QX-resistant oyster lines. HighlightsO_LIM. sydneyi infection induces a large transcriptional response in S. glomerata C_LIO_LIUpregulation of pathogen recognition genes, including galectins, occurs in infected tissues. C_LIO_LILack of differential expression of apoptosis genes suggests other immune strategies. C_LIO_LIG-protein coupled receptor pathways were upregulated, indicating species-specific responses. C_LIO_LIResults suggest possible suppression of host immune responses by the parasite. C_LI

zoology↗

Population-level whole genome sequencing of Ascochyta rabiei identifies genomic loci associated with isolate aggressiveness

Ascochyta blight caused by the ascomycete Ascochyta rabiei poses a major biotic threat to chickpea (Cicer arietinum) industries worldwide and incurs substantial costs to the Australian multimillion-dollar chickpea industry both in disease control and yield loss. The fungus was introduced to Australia in the 1970s from an unknown source population, and within a few decades, successfully established in all Australian agroecological chickpea growing regions. Although genetically highly clonal, a broad range of phenotypic variation in terms of aggressiveness exists among the Australian A. rabiei isolates. More recently, highly aggressive isolates capable of causing severe disease symptoms on moderate to highly resistant chickpea cultivars have increased in frequency. To identify genetic loci potentially associated with A. rabiei aggressiveness on Australian chickpea cultivars, we performed deep genome sequencing of 230 isolates collected from a range of agroecological chickpea growing regions between 2013 and 2020. Population genetic analyses using genome-wide single nucleotide polymorphism data identified three main clusters of genetically closely related isolates in Australia. Phylogenetic analyses showed that highly aggressive phenotypes developed multiple times independently throughout the phylogeny. Results point to minor contribution of multiple genetic regions and most likely epigenomic variations to aggressiveness of A. rabiei isolates on Australian chickpea cultivars. IMPACT STATEMENTThis research introduces new knowledge on the Australian A. rabiei population structure, molecular pathogenicity drivers and evolution as a clonal pathogen through comprehensive whole-genome sequencing approach. The knowledge generated on the structure and origin of the Australian A. rabiei and existence of only one mating type continues to inform researchers, growers, breeders and the broader industry on the importance for continued tight biosecurity measures and inform development of accurate and informed disease management and resistance breeding strategies. This research provides a rare real-life example to the effect of genetic drift on a clonal pathogen population and the importance of biosecurity to protect introduction from non-endemic isolates through seed importation in the current era of international markets. DATA SUMMARYAn online dataset containing the data and code required to reproduce the results found in this publication have been deposited at Zenodo (DOI 10.5281/zenodo.12575659). Isolate aggressiveness and collection metadata are available in the Ascochyta dashboard at http://bit.ly/asco-dashboard. Raw sequencing data used in this study was deposited to the NCBI Short Read Archive (SRA) and is available through BioProject PRJNA1175002. The authors confirm all supporting data, code and protocols have been provided within the article or through supplementary data files.

genomics↗

Transcriptomic stability or lability explains sensitivity to climate stressors in coralline algae

Crustose coralline algae (CCA) are a group of calcifying red macroalgae crucial to tropical coral reefs because they form crusts that cement together the reef framework1. Previous research into the responses of CCA to ocean warming (OW) and ocean acidification (OA) have found reductions in calcification rates and survival2,3, with magnitude of effect being species-specific. Responses of CCA to OW and OA could be linked to evolutionary divergence time and/or their underlying molecular biology, the role of either being unknown in CCA. Here we show Sporolithon durum, a species from an earlier diverged lineage that exhibits low sensitivity to climate stressors, had little change in metabolic performance and did not significantly alter the expression of any genes when exposed to temperature and pH perturbations. In contrast, Porolithon onkodes, a species from a recently diverged lineage, reduced photosynthetic rates and had over 400 significantly differentially expressed genes in response to experimental treatments, with differential regulation of genes relating to physiological processes. We suggest earlier diverged CCA may be resistant to OW and OA conditions predicted for 2100, whereas taxa from more recently diverged lineages with demonstrated high sensitivity to climate stressors may have limited ability for acclimatisation.

molecular biology↗

Current population structure and pathogenicity patterns of Ascochyta rabiei in Australia

Ascochyta blight disease, caused by the necrotrophic fungus Ascochyta rabiei, is a major biotic constraint to chickpea production in Australia and worldwide. Detailed knowledge of the structure of the pathogen population and its potential to adapt to our farming practices is key to informing optimal management of the disease. This includes understanding the molecular diversity among isolates and the frequency and distribution of the isolates that have adapted to overcome host resistance across agro-geographically distinct regions. Thanks to continuous monitoring efforts over the past six years, a comprehensive collection of A. rabiei isolates was collated from the major Australian production regions. To determine the molecular structure of the entire population, representative isolates from each collection year and growing region have been genetically characterised using a DArTseq genotyping-by-sequencing approach. The genotyped isolates were further phenotyped to determine their pathogenicity levels against a differential set of chickpea cultivars and genotype-phenotype associations were inferred. Overall, the Australian A. rabiei population displayed a far lower genetic diversity (average Neis gene diversity of 0.047) than detected in other populations worldwide. This may be explained by the presence of a single mating-type in Australia, MAT1-2, limiting its reproduction to a clonal mode. Despite the low detected molecular diversity, clonal selection appears to have given rise to a subset of adapted isolates that are highly pathogenic on commonly employed resistance sources, and that are occurring at an increasing frequency. To better understand the mechanisms and patterns of the pathogen adaptation, multi-locus genotype analysis was performed and two hypotheses were proposed on how new genotypes emerge. These were: 1) In a local, within-region evolutionary pathway; or 2) Through inter-region dispersal, most likely due to human activities. Furthermore, a cluster of genetically similar isolates was identified, with a higher proportion of highly aggressive isolates than in the general population, indicating the adaptive evolution of a sub-set of isolates that pose a greater risk to the chickpea industry. The discovery of distinct genetic clusters associated with high and low isolate pathogenicity forms the foundation for the development of a molecular pathotyping tool for the Australian A. rabiei population. Application of such a tool, along with continuous monitoring of the genetic structure of the population will provide crucial information for the screening of breeding material and integrated disease management packages. Data SummaryAn online dataset containing all supporting genotyping and phenotyping data and the code required to reproduce the results, summary tables and plots found in this publication, is publicly available at Zenodo via the following links: https://zenodo.org/record/4311477; DOI: 10.5281/zenodo.4311477 (1).

genomics↗

Evidence of recent increased pathogenicity within the Australian Ascochyta rabiei population

Ascochyta Blight (AB), caused by Ascochyta rabiei (syn Phoma rabiei), is the major endemic foliar fungal disease affecting the Australian chickpea industry, resulting with potential crop loss and management costs. This study was conducted to better understand the risk posed by the Australian A. rabiei population to current resistance sources and to provide informed decision support for chemical control strategies. Recent changes in the pathogenicity of the population were proposed based on disease severity and histopathological observations on a host set. Controlled environment disease screening of 201 isolates on the host set revealed distinct pathogenicity groups, with 41% of all isolates assessed as highly aggressive and a significant increase in the proportion of isolates able to cause severe damage on resistant and moderately resistant cultivars since 2013. In particular, the frequency of highly aggressive isolates on the widely adopted PBA HatTrick cultivar rose from 18% in 2013 to 68% in 2017. In addition, isolates collected since 2016 caused severe disease on Genesis 090, another widely adopted moderately resistant cultivar and on ICC3996, a commonly used resistance source. Of immediate concern was the 10% of highly aggressive isolates able to severely damage the recently released resistant cultivar PBA Seamer (2016). Histopathology studies revealed that the most aggressive isolates were able to germinate, develop appressoria and invade directly through the epidermis faster than lower aggressive isolates on all hosts assessed, including ICC3996. The fungal invasion triggered a common reactive oxygen species (ROS) and hypersensitive response (HR) on all assessed resistant genotypes with initial biochemical and subsequent structural defence responses initiated within 24 hours of inoculation by the most highly aggressive isolates. These responses were much faster on the less resistant and fastest on the susceptible check host, indicating that speed of recognition was correlated with resistance rating. This will inform fungicide application timing so that infected crops are sprayed with prophylactic chemistries prior to invasion and with systemic chemistries after the pathogen has invaded.Competing Interest StatementThe authors have declared no competing interest.View Full Text

plant biology↗