bioRxiv Science⌕ Search

bioRxiv · 10.64898/2026.03.14.711691

Multiple nuclei means multiple chromosome sets in Botrytis cinerea and Neurospora crassa

Abstract

We often think of fungi as mysterious organisms that do not follow the general principles of other eukaryotes. Thus, when exciting results are found, these organisms do not always receive the rigorous level of scrutiny seen in other fields. For many fungal species, dispersal and reproduction relies on spores, either sexual or asexual. These spores can either have a single nucleus, or multiple nuclei, and the purpose of these presumably mitotic copies was unclear. Recently it was described that the multiple nuclei in these spores are not mitotic duplicates, but instead they share a single haploid set of chromosomes distributed across nuclei. Here, we provide fluorescent microscopy and UV mutagenesis data that is inconsistent with this hypothesis. Contrasting these previous results, we observe multiple sets of chromosomes in spores of both B. cinerea and N. crassa. We also observed a strong linear relationship between the number of nuclei in spores and the total acriflavine fluorescence, further supporting mitotic copies. Genome sequencing of colonies arising from UV-irradiated colonies also recovered variants at intermediate frequences, instead of the fixed 100% expected from the new model proposed. This evidence suggests that, as long suspected, these nuclei are indeed mitotic copies, and that a re-evaluation of fungal biology is not currently necessary.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Zhang, D., van Kan, J. A. L., Auxier, B.. 2026-03-17. Multiple nuclei means multiple chromosome sets in Botrytis cinerea and Neurospora crassa. https://doi.org/10.64898/2026.03.14.711691

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

OPA1 controls mitochondrial dysfunction-driven liver fibrosis in MASLD

Progressive hepatic fibrosis is the principal determinant of morbidity and mortality in metabolic dysfunction-associated steatotic liver disease and steatohepatitis (MASLD/MASH). Mitochondrial dysfunction is a hallmark of MASH, and the release of mitochondrial damage-associated molecular patterns (mito-DAMPs) from injured hepatocytes can promote fibrosis. However, how mitochondrial dynamics and quality control shape the fibrotic response in MASLD/MASH remains unclear. Here, through large-scale genomic analyses of mitochondrial genes governing mitophagy, fusion and fission in human MASLD, with a power-equivalent sample size of approximately 700,000 individuals, we identify a strong association between hepatic fibrosis and the mitochondrial fusion factor dynamin-like GTPase optic atrophy 1 (OPA1). OPA1 transcripts and protein abundance in the liver epithelium were progressively dysregulated with advancing fibrosis. In mice, hepatocyte-specific OPA1 loss alone was sufficient to induce hepatic stellate cell activation and fibrosis in zone 3, promoted the release of mito-DAMPs into the circulation and exacerbated fibrosis in experimental MASH. These findings identify OPA1 as a central regulator of the hepatic fibrotic response and connect defective mitochondrial homeostasis to mito-DAMP release, hepatic stellate cell activation and fibrosis in MASLD.

genetics↗

Temporal control of mitochondrial mutagenesis reveals the fate of mtDNA mutations with age

Mutations in the mitochondrial genome (mtDNA) play a critical role in the aging process and a wide variety of age-related diseases. However, it remains unclear when the mutations that drive physiological decline arise. To answer this question, we generated a new mouse model in which mitochondrial mutagenesis can be confined to a defined window of time. Surprisingly, we found that mutations that arise during the first two months of life are sufficient to drive a wide variety of age-related pathologies, and that the severity of this pathology is broadly regulated by distinct, tissue-specific selective pressures that control the fate of mtDNA mutations with age. Further, we found that selection against deleterious variants can be modulated by manipulation of mitochondrial fusion in vitro and in vivo. These observations raise the possibility that in some tissues, the pace of aging is pre-determined by events that occur early in life and that interventions targeting mitochondrial fusion may be able to slow down or reverse the expansion of these pathogenic variants. These results carry far-reaching implications for strategies aimed at preventing or delaying age-related decline.

genetics↗

Innate immune stress pathway activation underlies heterochromatin dysfunction pathology

Heterochromatin loss disrupts nuclear architecture, gene regulation and repetitive element silencing, and is associated with diverse human diseases. However, mechanisms linking heterochromatin dysfunction to pathological phenotypes remain unclear. Using genetic interaction screening and genomic analyses in C. elegans, we identify secondary activation of the Intracellular Pathogen Response (IPR), an innate immune stress pathway, as a major contributor to heterochromatin mutant phenotypes. Constitutive IPR activation phenocopies slow growth and indirect transcriptional changes observed in these mutants. Depletion of genetic enhancers further increased, whereas suppressor RNAi attenuated IPR activation, with direct heterochromatin targets remaining substantially deregulated. Notably, many suppressors encode active chromatin components, and mild reduction of RNA polymerase II activity ameliorates growth defects in C. elegans HP1 mutants and human HP1-deficient cells. Our findings reveal secondary stress response activation as an important mechanism linking heterochromatin dysfunction to pathology and identify transcriptional dampening as a potential therapeutic strategy for mitigating these effects.

genetics↗