bioRxiv Science⌕ Search

Biology subjects

Corwin, J.

Publications and source records attributed to Corwin, J..

3 recordsLinked to original sources

The RNA helicase KREH2 directly binds the RESC1-RESC2 complex in trypanosomatid mitochondrial RNA editing

Trypanosomatids are medically important single-celled eukaryotic protists with exceptional RNA biology. They display highly unusual RNA biogenesis pathways, notably mitochondrial RNA editing, an essential post-transcriptional process transforming cryptic primary transcripts into functional mRNAs. Large multiprotein assemblies coordinate the RNA editing process, in which small guide RNAs (gRNAs) anneal to the pre-mRNAs and serve as templates for uridine insertion or deletion. Kinetoplast RNA Editing Helicases (KREHs) are important components of the RNA editing process that modifies large portions of pre-mRNA via the sequential annealing and dissociation of multiple gRNAs. However, how KREH helicases interact with components of the editing machinery, and which subunits mediate these interactions, remain unresolved. Here, we examined an association between the DEAH/RHA RNA helicase KREH2 and the RESC1-RESC2 protein heterodimer using proximity labeling and co-immunoprecipitation coupled to quantitative mass spectrometry in vivo. We reconstituted a minimal trimeric KREH2 peptide-RESC1-RESC2 complex in vitro and characterized novel direct binding of a KREH2 peptide to RESC1 using cryo-electron microscopy. These results establish a mechanistic link between the RNA helicase KREH2 and the RESC1-RESC2 module at the 5'-end of gRNAs, providing new avenues for studying the orchestration of RNA remodeling in trypanosomatid mitochondrial RNA editing.

molecular biology↗

A generalist pathogen view of plant evolution

Botrytis cinerea is a polyphagous fungal pathogen that causes necrotic disease on more than a thousand known hosts widely spread across the plant kingdom. While it is known that quantitative resistance in the host and quantitative virulence in the pathogen largely mediate this pathosystem, how this pathogen interacts with the extensive host diversity is unknown. Does this pathogen have quantitative virulence efficiency on all hosts or individual solutions for each host? To address this question, we generated an infectivity matrix of 98 strains of Botrytis cinerea on 90 genotypes representing eight host plants. This experimental infectivity matrix showed that the predominant sources of quantitative variation are between host species and among pathogen strains. Furthermore, the eight eudicot hosts interacted individually with Botrytis cinerea strains independently of the evolutionary relatedness between hosts. An additive quantitative model can explain the complexity of these interactions in which Botrytis host specificity and general virulence have distinct polygenic architectures.

plant biology↗

Resequencing and association mapping of the generalist pathogen Botrytis cinerea

We performed whole genome resequencing of 84 field isolates of Botrytis cinerea, largely collected from a local set of plant species. Combined with 13 previously resequenced isolates sampled from diverse locations, this gave a collection of 97 isolates for studies of natural variation. Alignment to the reference sequence T4 and SNP detection provided further data for population genetics analysis including a mapping population for association studies. Although much of the genomic diversity was captured in the original 13 isolates, the additional genomes increased total diversity in the population by a third. Surprisingly, the same additional genomes increase mitochondrial diversity 2-fold. Across the population, LD was limited and decayed rapidly, reflecting frequent outcrossings. Effectively, this sampling strategy increased the level of genetic diversity available, whilst limiting the problem of population stratification and enabling GWAS of several phenotypes on common Arabidopsis plants affected in disease pathways. Overlap of results using all GWAS methods revealed numerous candidate genes / pathways that potentially contribute to its broad host range and offer conceivable pathogen decrease targets.

genomics↗