Biology subjects

Barragan, A. C.

Publications and source records attributed to Barragan, A. C..

6 recordsLinked to original sources

bioRxiv2024

Multiple horizontal mini-chromosome transfers drive genome evolution of clonal blast fungus lineages

Crop disease pandemics are often driven by clonal lineages of plant pathogens that reproduce asexually. How these clonal pathogens continuously adapt to their hosts despite harboring limited genetic variation, and in absence of sexual recombination remains elusive. Here, we reveal multiple instances of horizontal chromosome transfer within pandemic clonal lineages of the blast fungus Magnaporthe (Syn. Pyricularia) oryzae. We identified a horizontally transferred 1.2Mb supernumerary mini-chromosome which is remarkably conserved between M. oryzae isolates from both the rice blast fungus lineage and the lineage infecting Indian goosegrass (Eleusine indica), a wild grass that often grows in the proximity of cultivated cereal crops. Furthermore, we show that this mini-chromosome was horizontally acquired by clonal rice blast isolates through at least nine distinct transfer events over the past three centuries. These findings establish horizontal mini-chromosome transfer as a mechanism facilitating genetic exchange among different host-associated blast fungus lineages. We propose that blast fungus populations infecting wild grasses act as genetic reservoirs that drive genome evolution of pandemic clonal lineages that afflict cereal crops.

evolutionary biology↗

bioRxiv2022

Wild grass isolates of Magnaporthe (Syn. Pyricularia) spp. from Germany can cause blast disease on cereal crops

Pathogens that cause destructive crop diseases often infect wild host plants. However, surveys of major plant pathogens tend to be skewed towards cultivated crops and often neglect the wild hosts. Here, we report an emerging disease threat generated by the blast fungus Magnaporthe (Syn. Pyricularia) spp. in central Europe. We found that this notoriously devastating plant pathogen infects the wild grasses foxtail millet (Setaria spp.) and crabgrass (Digitaria spp.) in south-western Germany, a region previously deemed unfavorable for blast disease. Using phenotypic characterization and genomic analyses, we determined that the observed disease symptoms are associated with the Setaria spp.-infecting lineage of M. oryzae and its sister species Magnaporthe grisea. We showed that M. oryzae isolates can infect barley and wheat, thus highlighting the risk of pathogen spread to crops. In addition, M. oryzae isolates which co-occur in natural populations display compatible mating types and variable candidate effector gene content, which may enhance the pathogens adaptive potential. Our findings stress the risk of blast fungus infections expanding into European cereal crops through migration and host jumps. This underlines the importance for pathogen surveillance not only on cultivated crops, but also on wild host plants. Author SummaryWild plant species are often overlooked during pathogen virulence surveys. However, many of the diseases we observe in crops are a consequence of host jumps from wild to cultivated plant species. This is reminiscent of zoonotic diseases, where host jumps from wild animals to humans result in new disease outbreaks. Here, we report that the notoriously devastating blast fungus Magnaporthe (Syn. Pyricularia) spp. occurs on wild grasses in south-western Germany. This region, which is at the center of the European cereal belt, has so far been viewed as having unfavorable climatic conditions for the blast disease. The newly identified blast fungus isolates have the capacity to infect wheat and barley cultivars, highlighting the risk of the disease spreading to staple cereal crops. In addition, there is potential for sexual recombination in local populations, which may increase the evolutionary potential of the fungus and might facilitate host jumps to cereal crops. Our findings emphasize the urgent need for surveillance of plant diseases on both wild hosts and crops.

plant biology↗

bioRxiv2021

TSC2-extracellular matrix crosstalk controls pulmonary vascular proliferation and pulmonary hypertension

Increased proliferation and survival of resident cells in small pulmonary arteries (PA) are important drivers of pulmonary hypertension (PH). Tuberous sclerosis complex 2 (TSC2) is a negative regulator of mTOR complex 1 and cell growth. Here we show that TSC2 is deficient in small remodeled PA/PA vascular smooth muscle cells (PAVSMC) from human PAH and experimental PH lungs. TSC2 deficiency was reproduced in vitro by maintaining PAVSMC on pathologically stiff substrates and was required for stiffness-induced proliferation, accumulation of transcriptional co-activators YAP/TAZ and up-regulation of mTOR. Depletion of TSC2 reproduced PH features in vitro in human PAVSMC and in vivo in SM22-Tsc2+/- mice. TSC2 loss in PAVSMC was supported by YAP and led to the up-regulation of YAP/TAZ and mTOR via modulating the extracellular matrix (ECM) composition. ECM, produced by TSC2-deficient PAVSMC, promoted growth of non-diseased PA adventitial fibroblasts and PAVSMC, which, in turn, was prevented by 5{beta}1 integrin receptor antagonist ATN161. In vitro, molecular and pharmacological (SRT2104) restoration of TSC2 down-regulated YAP/TAZ, mTOR, and ECM production, inhibited proliferation and induced apoptosis in human PAH PAVSMC. In vivo, orally administrated SRT2104 restored TSC2, resolved pulmonary vascular remodeling, PH, and improved right heart in two rodent models of PH. Thus, PAVSMC TSC2 is a critical integrator of ECM composition and stiffness with pro-proliferative signaling and PH, and the restoration of functional TSC2 could be an attractive therapeutic option to treat PH. One Sentence SummaryTSC2 acts as mechanosensor and mechanotransducer, integrating ECM composition and stiffness with pro-proliferative signaling in pulmonary vasculature; its deficiency in PA vascular smooth muscle cells results in ECM remodeling, hyper-proliferation and pulmonary hypertension, which could be reversed by pharmacological restoration of functional TSC2.

molecular biology↗

bioRxiv2021

Small peptides modulate the immune function of the ion channel-like protein ACD6 in Arabidopsis thaliana

ACCELERATED CELL DEATH 6 (ACD6) mediates a trade-off between growth and defense in Arabidopsis thaliana. However, the precise biochemical mechanism by which ACD6 and related proteins in plants act remains enigmatic. Here, we identified two loci, MODULATOR OF HYPERACTIVE ACD6 1 (MHA1) and its paralog MHA1-LIKE (MHA1L), that code for [~]7 kDa proteins that differentially interact with specific ACD6 variants. MHA1L enhances accumulation of an ACD6 complex, thereby increasing activity of the ACD6 standard allele for regulating plant growth and defenses. ACD6 is a multipass transmembrane protein with intracellular ankyrin repeats that are structurally similar to those found in mammalian ion channels. Several lines of evidence link increased ACD6 activity to enhanced calcium influx, likely mediated by ACD6 itself and with MHA1L as a direct regulator of ACD6.

plant biology↗

bioRxiv2021

Homozygosity at its Limit: Inbreeding Depression in Wild Arabidopsis arenosa Populations

New combinations of genetic material brought together through hybridization can lead to unfit offspring as a result of outbreeding or inbreeding depression. In selfing plants such as Arabidopsis thaliana, outbreeding depression is typically the result of pairwise deleterious epistatic interactions between two alleles that can geographically co-occur. What remains elusive is how often alleles resulting in genetic incompatibilities co-occur in natural populations of outcrossing plant species. To address this question, we screened over two thousand five hundred wild Arabidopsis arenosa hybrid plants in search for potential genetic mismatches. We show that although abnormal deleterious phenotypes are common, the transcriptional profiles of these abnormal A. arenosa plants differ substantially from those seen in incompatible A. thaliana hybrids. The abnormal hybrid phenotypes in A. arenosa had different underlying genetic architectures, yet a repeated theme was increased homozygosity, indicating that inbreeding rather than outbreeding depression gives rise to some of the deleterious phenotypes segregating in wild A. arenosa populations.

plant biology↗

bioRxiv2020

A singleton NLR of recent origin causes hybrid necrosis in Arabidopsis thaliana

Hybrid necrosis in plants arises from conflict between divergent alleles of immunity genes contributed by different parents, resulting in autoimmunity. We investigate a severe hybrid necrosis case in Arabidopsis thaliana, where the hybrid does not develop past the cotyledon stage and dies three weeks after sowing. Massive transcriptional changes take place in the hybrid, including the upregulation of most NLR disease resistance genes. This is due to an incompatible interaction between the singleton TIR-NLR gene DANGEROUS MIX 10 (DM10), which was recently relocated from a larger NLR cluster, and an unlinked locus, DANGEROUS MIX 11 (DM11). There are multiple DM10 allelic variants in the global A. thaliana population, several of which have premature stop codons. One of these, which has a truncated LRR domain, corresponds to the DM10 risk allele. The DM10 locus and the adjacent genomic region in the risk allele carriers are highly differentiated from those in the non-risk carriers in the global A. thaliana population, suggesting that this allele became geographically widespread only relatively recently. The DM11 risk allele is much rarer and found only in two accessions from southwestern Spain - a region from which the DM10 risk haplotype is absent - indicating that the ranges of DM10 and DM11 risk alleles may be non-overlapping.

evolutionary biology↗