Author contributions DCJ coordinated all analyses, isolated DNA for sequencing, analysed and filtered SNP calls, conducted diversity analysis and GWAS and drafted the manuscript. CR produced phenotype data for growth on various solid media and growth rates in liquid media. AR conducted analysis of dating using mitochondrial data. DS conducted GWAS. MP analysed all phenotype data. TM identified LTR transposon insertions and analysed transposon insertion data. FXM conducted crosses for analysis of spore viability ZI produced indel calls with Cortex. WL conducted analysis of recombination rate, linkage disequilibrium decay and PCA for distance between strains. TMKC assisted with phenotype and population analysis. RP analysed Cortex and GATK indel calls. MM conducted amino acid profiling. JLDL and AC produced automated measures of cell morphology. SB aligned reads and produced GATK SNP calls. GH analysed population structure using fineSTRUCTURE. BO'F estimated the TMRCA from the nuclear genome using ACG. TK identified LTR transposon insertions JTS produced de novo assemblies. LB developed the custom Workspace workflow Spotsizer. BT assisted with sequence analysis. DAB assisted with analysis of novel genes. TS assisted with strain verification. SC produced images of wild strains and assisted with strain verification. JEEUH assisted with SNP validation. LvT and MT assisted with LTR validation. LJ and JL assisted with manual measures of cell morphology and FACS. SA produced gene expression data. MF, KM and ND assisted with sequencing. WB initiated and assisted with strain collection. JH coordinated manual measures of cell morphology and FACS. RECS coordinated automated measures of cell morphology. MR coordinated amino acid profiling. NM conducted analysis of recombination, linkage disequilibrium and advised on aspects of diversity and GWAS. DJB advised on GWAS. RD facilitated sequencing. JB contributed to the initiation and development of the project and financed the JB laboratory. AccessionsSequence data are archived in the European Nucleotide Archive (www.ebi.ac.uk/ena/), Study Accessions PRJEB2733 and PRJEB6284 (Supplementary Table 7). All SNPs and indels were submitted to NCBI dbSNP (www.ncbi.nlm.nih.gov/SNP/). Accessions are 974514578-974688138 (SNPs) and 974702618-974688139 (indels). Europe PMC Funders Group AbstractNatural variation within species reveals aspects of genome evolution and function. The fission yeast Schizosaccharomyces pombe is an important model for eukaryotic biology, but researchers typically use one standard laboratory strain. To extend the utility of this model, we surveyed the genomic and phenotypic variation in 161 natural isolates. We sequenced the genomes of all strains, revealing moderate genetic diversity (π = 3 ×10 −3 ) and weak global population structure. We estimate that dispersal of S. pombe began within human antiquity (~340 BCE), and ancestors of these strains reached the Americas at ~1623 CE. We quantified 74 traits, revealing substantial heritable phenotypic diversity. We cond...
Our current understanding of how natural genetic variation affects gene expression beyond well-annotated coding genes is still limited. The use of deep sequencing technologies for the study of expression quantitative trait loci (eQTLs) has the potential to close this gap. Here, we generated the first recombinant strain library for fission yeast and conducted an RNA-seq-based QTL study of the coding, non-coding, and antisense transcriptomes. We show that the frequency of distal effects (trans-eQTLs) greatly exceeds the number of local effects (cis-eQTLs) and that non-coding RNAs are as likely to be affected by eQTLs as protein-coding RNAs. We identified a genetic variation of swc5 that modifies the levels of 871 RNAs, with effects on both sense and antisense transcription, and show that this effect most likely goes through a compromised deposition of the histone variant H2A.Z. The strains, methods, and datasets generated here provide a rich resource for future studies.
What is the nature of the ageing process? What is the spore survival, that one would expect upon analysing a self-cross, in a wild fission yeast strain? Could this two research questions be, somehow, related? In this manuscript, I am describing some interesting observations obtained while studying fission yeast spore survival values upon genetic crosses. Early findings brought my attention into mainly studying self-crosses (intra-strain crosses in which any cell can be involved in by matting with a sibling cell). This study, yield some interesting findings. As a summary: 1) most fission yeast self-crosses do show low spore survival values; 2) clonally related strains show a high phenotypic variability in self-cross spore survival values; 3) differences in self-cross spore survival values can be detected when comparing zygotic and azygotic mattings; 4) self-cross spore survival values are highly affected by environmental factors, mainly producing a reduction in the spore survival values; 5) self-cross spore survival values are "recovered" when cells are subjected to several rounds of meiotic divisions; 6) signs of correlation between spore survival and vegetative cell survival (prior to the entry into meiosis) have been observed in this study.All those observations, among others, are discussed as part of an epigenetic variability that exist in fission yeast populations. A cyclical behaviour, of this epigenetic variability it is proposed, defining an underlying ratchet-like epigenetic mechanisms acting in all cells. In
In fission yeast, mating-type switching involves replacing genetic information contained at the expressed mat1 locus by that of either the mat2P or mat3M donor loci. Donor selection is nonrandom, as mat1P cells preferentially use mat3M for switching, whereas mat1M cells use mat2P. Switching directionality is determined by the cell-typespecific distribution of the Swi2-Swi5 complex that, in mat1P cells, localises to mat3M and, only in mat1M cells, spreads to mat2P in a heterochromatin-dependent manner. Mechanisms regulating spreading of Swi2-Swi5 across heterochromatin are not fully understood. Here, we show that the fission yeast homologue of CENP-B, Abp1, binds to the silent domain of the mating-type locus and regulates directionality of switching. Deletion of abp1 prevents utilisation of mat2P, as when heterochromatin is disrupted and spreading of Swi2-Swi5 is impaired. Our results show that, indeed, deletion of abp1 abolishes spreading of Swi2-Swi5 to mat2P. However, in abp1D cells, heterochromatin organisation at the mating-type locus is preserved, indicating that Abp1 is actually required for efficient spreading of Swi2-Swi5 through heterochromatin. Cbh1 and Cbh2, which are also homologous to CENP-B, have only a minor contribution to the regulation of directionality of switching, which is in contrast with the strong effects observed for Abp1.
Network analysis provides a powerful framework for the interpretation of genome-wide data. While static network approaches have proved fruitful, there is increasing interest in the insights gained from the analysis of cellular networks under different conditions. In this work, we study the effect of stress on cellular networks in fission yeast. Stress elicits a sophisticated and large scale cellular response, involving a shift of resources from cell growth and metabolism towards protection and maintenance. Previous work has suggested that these changes can be appreciated at the network level. In this paper, we study two types of cellular networks: gene co-regulation networks and weighted protein interaction networks. We show that in response to oxidative stress, the co-regulation networks re-organize towards a more modularised structure: while sets of genes become more tightly co-regulated, co-regulation between these modules is decreased. This shift translates into longer average shortest path length, increased transitivity, and decreased modular overlap in these networks. We also find a similar change in structure in the weighted protein interaction network in response to both oxidative stress and nitrogen starvation, confirming and extending previous findings. These changes in network structure could represent an increase in network robustness and/or the emergence of more specialised functional modules. Additionally, we find stress induces tighter co-regulation of non-coding RNAs, decreased functional importance of splicing factors, as well as changes in the centrality of genes involved in chromatin organization, cytoskeleton organization, cell division, and protein turnover.
In this paper I would like to introduce some theoretical considerations, which, if proven right by the experimental frameworks designed to test them, might stand for a paradigmatic change on genetics, genomics and ageing studies. This paper further develops a theoretical framework previously proposed by this author (Marsellach, 2017). Despite this, this paper is written as a standalone paper, which describe in more detail the previously hinted model (Marsellach, 2017), and adds emphasis in the putative implications that, the proposed theoretical framework, might have in describing the way in which the epigenetic information is transmitted from one generation to the following ones, and in the implications that this might have for genetics, genomics and ageing studies.
Multi-KH domain proteins are highly evolutionarily conserved proteins that associate to polyribosomes and participate in RNA metabolism. Recent evidence indicates that multi-KH domain proteins also contribute to the structural organization of heterochromatin both in mammals and Drosophila. Here, we show that the multi-KH domain protein of Saccharomyces cerevisiae, Scp160p, contributes to silencing at telomeres and at the mating-type locus, but not to ribosomal silencing. The contribution of Scp160p to silencing is independent of its binding to the ribosome as deletion of the last two KH domains, which mediate ribosomal binding, has no effect on silencing. Disruption of SCP160 increases cell ploidy but this effect is also independent of the contribution of Scp160p to telomeric silencing as strong relief of silencing is observed in ⌬scp160 cells with normal ploidy and, vice versa, ⌬scp160 cells with highly increased ploidy show no significant silencing defects. The TPE phenotype of ⌬scp160 cells associates to a decreased Sir3p deposition at telomeres and, in good agreement, silencing is rescued by SIR3 overexpression and in a ⌬rif1⌬rif2 mutant. Scp160p shows a distinct perinuclear localization that is independent of its ability to bind ribosomes. Moreover, telomere clustering at the nuclear envelope is perturbed in ⌬scp160 cells and disruption of the histone deacetylase RPD3, which is known to improve telomere clustering, rescues telomeric silencing in ⌬scp160 cells. These results are discussed in the context of a model in which Scp160p contributes to silencing by helping telomere clustering.Multi-KH domain proteins are highly evolutionarily conserved proteins that have been described in all eukaryotic organisms analyzed to date from the yeast Saccharomyces cerevisiae (Scp160p) and Schizosaccharomycespombe to nematodes, Drosophila (DDP1), and vertebrates (vigilin) (1-6). All these proteins are characterized by the presence of multiple KH domains that are organized in tandem. The KH domain is a single-stranded nucleic acid binding motif that, first identified in the RNA-binding protein hnRNPK, has been found in a number of proteins binding single-stranded nucleic acids (7). Consistent with this molecular organization, several multi-KH domain proteins have been shown to bind single-stranded nucleic acids with high affinity, in vitro. Multi-KH domain proteins were proposed to participate in different aspects of RNA metabolism from the interaction with specific mRNAs (1, 8) to tRNA export and the general regulation of mRNA translation and protein synthesis (9 -12). In particular, in S. cerevisiae, Scp160p is found associated to both soluble and membranebound polyribosomes (13-15). Binding of Scp160p to ribosomes requires the C-terminal region so that, a truncated protein missing the last two KH domains is not capable of binding ribosomes (16,17). Also in human cells, vigilin associates to ribosomes through its C-terminal domain (18) and localizes to the rough endoplasmic reticulum (RER) 4 (19). Consistent with an asso...
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.