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Sordaria macrospora wild type and developmental mutant delta-asf1

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Sordaria macrospora

PROVIDER: GSE216634 | GEO | 2023/11/20

REPOSITORIES: GEO

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Hi-C analysis of the Sordaria macrospora wild type and developmental mutant delta-asf1 [HiC]

Project description:Chromatin organization of the wild type and delta-asf1 mutant of the filamentous ascomycete Sordaria macrospora was analyzed by Hi-C. The delta-asf1 mutant lacks the conserved histone chaperone ASF1 and is unable to produce sexual fruiting bodies. It was hypothesized that the lack of the histone chaperone ASF1 in the mutant might lead to differences in short- or long-distance interactions of chromatin. Furthermore, it was hypothesized that chromatin organization might change during sexual development in the wild type as a prerequisite for the drastic transcriptome changes during development that were observed in earlier studies.

2023-11-20 | GSE216632 | GEO

ChIP-seq analysis of the Sordaria macrospora wild type and the developmental mutant delta-asf1

Project description:Genome-wide distribtuion of histone H3K56ac (histone H3 acetylated at lysine 56) was analyzed in the wild type and the sterile mutant asf1. The asf1 gene encodes a conserved histone chaperone, and preliminary experimentes indicated changes in histone modifications in the mutant that were analyzed on a genome-wide basis in these experiments.

2023-11-20 | GSE228529 | GEO

ChIP-seq analysis of the Sordaria macrospora wild type and the developmental mutant delta-asf1 [ChIP-seq]

Project description:Genome-wide distribtuion of histone H3 and H3K27me3 (histone H3 tri-methylated at lysine 27) was analyzed in the wild type and the sterile mutant asf1. The asf1 gene encodes a conserved histone chaperone, and preliminary experimentes indicated changes in histone modifications in the mutant that were analyzed on a genome-wide basis in these experiments.

2023-11-20 | GSE216629 | GEO

Bisulfite sequencing of Sordaria macrospora wild type and asf1 mutant

Project description:The aim of this analysis was to analyze DNA methylation in the wild type and the histone chaperone mutant asf1 of the filamentous fungus Sordaria macrospora.

2018-11-26 | GSE114029 | GEO

MNase-seq analysis of wild type and asf1 mutant of Sordaria macrospora

Project description:The aim of this analysis was to analyze nucleosome distribution in the filamentous ascomycete Sordaria macrospora by micrococcal nuclease digestion and sequencing.

2018-11-26 | GSE92461 | GEO

Bisulfite sequencing of Sordaria macrospora wild type and asf1 mutant

Project description:Bisulfite sequencing of Sordaria macrospora wild type and asf1 mutant

| PRJNA454909 | ENA

Whole-Genome Sequencing of Sordaria macrospora Mutants Identifies Developmental Genes.

Project description:The study of mutants to elucidate gene functions has a long and successful history; however, to discover causative mutations in mutants that were generated by random mutagenesis often takes years of laboratory work and requires previously generated genetic and/or physical markers, or resources like DNA libraries for complementation. Here, we present an alternative method to identify defective genes in developmental mutants of the filamentous fungus Sordaria macrospora through Illumina/Solexa whole-genome sequencing. We sequenced pooled DNA from progeny of crosses of three mutants and the wild type and were able to pinpoint the causative mutations in the mutant strains through bioinformatics analysis. One mutant is a spore color mutant, and the mutated gene encodes a melanin biosynthesis enzyme. The causative mutation is a G to A change in the first base of an intron, leading to a splice defect. The second mutant carries an allelic mutation in the pro41 gene encoding a protein essential for sexual development. In the mutant, we detected a complex pattern of deletion/rearrangements at the pro41 locus. In the third mutant, a point mutation in the stop codon of a transcription factor-encoding gene leads to the production of immature fruiting bodies. For all mutants, transformation with a wild type-copy of the affected gene restored the wild-type phenotype. Our data demonstrate that whole-genome sequencing of mutant strains is a rapid method to identify developmental genes in an organism that can be genetically crossed and where a reference genome sequence is available, even without prior mapping information.

| S-EPMC3284333 | biostudies-literature

Sordaria macrospora strain:wild type SN1693

Project description:Sordaria macrospora strain:wild type SN1693 Genome sequencing and assembly

| PRJNA744349 | ENA

Gene expression in developmental mutants of Sordaria macrospora

Project description:The aim of this analysis was to analyze gene expression in developmental mutants of the filamentous ascomycete Sordaria macrospora. RNA was isolated from total mycelia, or young fruiting bodies (protoperithecia) were isolated by laser microdissection and RNA was extracted, amplified and used for RNA-sequencing.

2018-11-26 | GSE92337 | GEO

<i>Sordaria macrospora</i> Sterile Mutant pro34 Is Impaired in Respiratory Complex I Assembly.

Project description:The formation of fruiting bodies is a highly regulated process that requires the coordinated formation of different cell types. By analyzing developmental mutants, many developmental factors have already been identified. Yet, a complete understanding of fruiting body formation is still lacking. In this study, we analyzed developmental mutant pro34 of the filamentous ascomycete Sordaria macrospora. Genome sequencing revealed a deletion in the pro34 gene encoding a putative mitochondrial complex I assembly factor homologous to Neurospora crassa CIA84. We show that PRO34 is required for fast vegetative growth, fruiting body and ascospore formation. The pro34 transcript undergoes adenosine to inosine editing, a process correlated with sexual development in fruiting body-forming ascomycetes. Fluorescence microscopy and western blot analysis showed that PRO34 is a mitochondrial protein, and blue-native PAGE revealed that the pro34 mutant lacks mitochondrial complex I. Inhibitor experiments revealed that pro34 respires via complexes III and IV, but also shows induction of alternative oxidase, a shunt pathway to bypass complexes III and IV. We discuss the hypothesis that alternative oxidase is induced to prevent retrograde electron transport to complex I intermediates, thereby protecting from oxidative stress.

| S-EPMC9605262 | biostudies-literature

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