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Biology subjects

Anderson, J. B.

Publications and source records attributed to Anderson, J. B..

5 recordsLinked to original sources

Bowel dysmotility and enteric neuron degeneration in lysosomal storage disease mice is prevented by gene therapy

Background and aimsChildren with neurodegenerative disease often have debilitating gastrointestinal (GI) symptoms that may be due at least in part to underappreciated involvement of neurons in the enteric nervous system (ENS), the master regulator of bowel function. MethodsWe investigated bowel motility in mouse models of CLN1 and CLN2 disease, neurodegenerative lysosomal storage disorders caused by deficiencies in palmitoyl protein thioesterase-1 (PPT1) and tripeptidyl peptidase-1 (TPP1), respectively. We then explored the integrity of ENS anatomy in immunostained bowel wholemount preparations from these mice. Lastly, we administered adeno-associated viral gene therapy to neonatal mice and determined if this would prevent these newly identified bowel phenotypes. ResultsMouse models of CLN1 and CLN2 disease both displayed slow bowel transit in vivo that worsened with age. Although the ENS appeared to develop normally, there was a progressive and profound loss of myenteric plexus neurons accompanied by changes in enteric glia in adult mice. Neonatal administration of adeno-associated virus-mediated gene therapy prevented bowel transit defects and the loss of many ENS neurons. ConclusionsWe show that two neurodegenerative lysosomal storage diseases cause profound and progressive damage to the mouse enteric nervous system and impair bowel motility. We also provide proof-of-principle evidence that gene therapy can prevent enteric nervous system disease. This study may have general therapeutic implications for many inherited neurodegenerative disorders. What you need to knowO_ST_ABSBackground and ContextC_ST_ABSMany pediatric central nervous system disorders also have debilitating gastrointestinal symptoms. For most of these diseases, it is not known if the enteric nervous system (ENS) is also affected and to what degree ENS defects contribute to GI symptoms. To date, no attempts have been made to directly treat or prevent enteric nervous system disease via gene therapy. New FindingsThe enteric nervous system is severely affected in mouse models of CLN1 and CLN2 disease, profoundly neurodegenerative lysosomal storage disorders. Bowel transit defects and most of the enteric nervous system pathology can be prevented by neonatal administration of gene therapy. LimitationsInformation about enteric nervous system disease in human children is still lacking, and methods will need to be developed to treat the human bowel. ImpactThese findings identify an underappreciated effect of neurodegenerative disease upon the bowel and demonstrate that enteric nervous system degeneration can be prevented in mice. This provides a new perspective on these childhood disorders that may be applicable to many other conditions that affect the bowel. Lay SummaryIn childrens diseases where the brain degenerates, nerve cells in the bowel also die causing gastrointestinal problems, but this can be prevented by gene therapy.

neuroscience↗

The humungous fungus of Michigan three decades on

In the late 1980s, a genetic individual of the fungus Armillaria gallica that extended over at least 37 hectares of forest floor and encompassed hundreds of tree root systems was discovered on the Upper Peninsula of Michigan. Based on observed growth rates, the individual was estimated to be at least 1500 years old with a mass of more than 105 kg. Nearly three decades on, we returned to the site of individual for new sampling. We report here that the same genetic individual of A. gallica is still alive on its original site, but we estimated that it is older and larger than originally estimated, at least 2,500 years and 4 x 105 kg, respectively. We also show that mutation has occurred within the somatic cells of the individual, reflecting its historical pattern of growth from a single point. The overall rate of mutation, however, was extremely low. The large individual of A. gallica has been remarkably resistant to genomic change as it has persisted in place.

evolutionary biology↗

Persistence of Resident and Transplanted Genotypes of the Undomesticated Yeast, Saccharomyces paradoxus in Forest Soil

One might expect yeasts in soil to be highly dispersed via water or insects, forming ephemeral, genetically heterogeneous populations subject to competition and environmental stochasticity. Here, we report years-long persistence of genotypes of the yeast Sacchaormyces paradoxus in space and time. Within 1 km2 in a mixed hardwood forest on scales from centimeters to tens of meters, we detect persistence over 3 years of native genotypes, identified by SNPs genome-wide, of the wild yeast, Saccharomyces paradoxus around Quercus rubra and Q. alba. Yeasts were recovered by enrichment in ethanol-containing medium, which measures only presence or absence, not abundance. Additional transplantation experiments employed strains marked with spontaneous defects in the URA3 gene, which also confer resistance to 5-Fluoroorotic acid (5FOA). Plating soil suspensions from transplant sites on 5FOA medium permitted one-step quantification of yeast colony-forming units, with no interference from other unmarked yeasts or microorganisms. After an initial steep decrease in abundance, the yeast densities fluctuated over time, increasing in association with rainfall and decreasing in association with drought. After 18 months, the transplanted yeasts remain in place on the nine sites. In vitro transplantation experiments into non-sterile soil in petri dishes showed similar patterns of persistence and response to moisture and drought. To determine whether S. cerevisiae, not previously recovered from soils regionally, can persist in our cold-climate sites, we transplanted marked S. cerevisiae alone and in mixture with S. paradoxus in fall, 2017. Five months on, S. cerevisiae persist to the same extent as S. paradoxus.

ecology↗

Genome expansion and lineage-specific genetic innovations in the world’s largest organisms (Armillaria)

Armillaria species are both devastating forest pathogens and some of the largest terrestrial organisms on Earth. They forage for hosts and achieve immense colony sizes using rhizomorphs, root-like multicellular structures of clonal dispersal. Here, we sequenced and analyzed genomes of four Armillaria species and performed RNA-Seq and quantitative proteomic analysis on seven invasive and reproductive developmental stages of A. ostoyae. Comparison with 22 related fungi revealed a significant genome expansion in Armillaria, affecting several pathogenicity-related genes, lignocellulose degrading enzymes and lineage-specific genes likely involved in rhizomorph development. Rhizomorphs express an evolutionarily young transcriptome that shares features with the transcriptomes of fruiting bodies and vegetative mycelia. Several genes show concomitant upregulation in rhizomorphs and fruiting bodies and shared cis-regulatory signatures in their promoters, providing genetic and regulatory insights into complex multicellularity in fungi. Our results suggest that the evolution of the unique dispersal and pathogenicity mechanisms of Armillaria might have drawn upon ancestral genetic toolkits for wood-decay, morphogenesis and complex multicellularity.

evolutionary biology↗

Fungus causing White-Nose Syndrome in bats accumulates genetic variability in North America and shows no sign of recombination

Emerging fungal diseases of wildlife are on the rise worldwide (3) and the best lens on the evolution of the fungal pathogens is population genomics. Our genome-wide analysis shows that the newly introduced North American population of Pseudogymnoascus destructans, the causal agent of White-Nose Syndrome (WNS) in bats, has expanded in size, has begun to accumulate variation through mutation, and presents no evidence as yet for genetic exchange and recombination among individuals.

evolutionary biology↗