Differential paralog divergence modulates evolutionary outcomes in yeast
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PROVIDER: PRJNA344847 | ENA |
REPOSITORIES: ENA
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Project description:Evolutionary outcomes depend not only on the selective forces acting upon a species, but also on the genetic background. However, large timescales and uncertain historical selection pressures can make it difficult to discern such important background differences between species. Experimental evolution is one tool to compare evolutionary potential of known genotypes in a controlled environment. Here we utilized a highly reproducible evolutionary adaptation in Saccharomyces cerevisiae to investigate whether experimental evolution of other yeast species would select for similar adaptive mutations. We evolved populations of S. cerevisiae, S. paradoxus, S. mikatae, S. uvarum, and interspecific hybrids between S. uvarum and S. cerevisiae for 200-500 generations in sulfate-limited continuous culture. Wild-type S. cerevisiae cultures invariably amplify the high affinity sulfate transporter gene, SUL1. However, while amplification of the SUL1 locus was detected in S. paradoxus and S. mikatae populations, S. uvarum cultures instead selected for amplification of the paralog, SUL2. We measured the relative fitness of strains bearing deletions and amplifications of both SUL genes from different species, confirming that, converse to S. cerevisiae, S. uvarum SUL2 contributes more to fitness in sulfate limitation than S. uvarum SUL1. By measuring the fitness and gene expression of chimeric promoter-ORF constructs, we were able to delineate the cause of this differential fitness effect primarily to the promoter of S. uvarum SUL1. Our data show evidence of differential sub-functionalization among the sulfur transporters across Saccharomyces species through recent changes in noncoding sequence. Furthermore, these results show a clear example of how such background differences due to paralog divergence can drive changes in genome evolution.
2016-09-30 | GSE87401 | GEO
Project description:Evolutionary outcomes depend not only on the selective forces acting upon a species, but also on the genetic background. However, large timescales and uncertain historical selection pressures can make it difficult to discern such important background differences between species. Experimental evolution is one tool to compare evolutionary potential of known genotypes in a controlled environment. Here we utilized a highly reproducible evolutionary adaptation in Saccharomyces cerevisiae to investigate whether experimental evolution of other yeast species would select for similar adaptive mutations. We evolved populations of S. cerevisiae, S. paradoxus, S. mikatae, S. uvarum, and interspecific hybrids between S. uvarum and S. cerevisiae for ~200-500 generations in sulfate-limited continuous culture. Wild-type S. cerevisiae cultures invariably amplify the high affinity sulfate transporter gene, SUL1. However, while amplification of the SUL1 locus was detected in S. paradoxus and S. mikatae populations, S. uvarum cultures instead selected for amplification of the paralog, SUL2. We measured the relative fitness of strains bearing deletions and amplifications of both SUL genes from different species, confirming that, converse to S. cerevisiae, S. uvarum SUL2 contributes more to fitness in sulfate limitation than S. uvarum SUL1. By measuring the fitness and gene expression of chimeric promoter-ORF constructs, we were able to delineate the cause of this differential fitness effect primarily to the promoter of S. uvarum SUL1. Our data show evidence of differential sub-functionalization among the sulfate transporters across Saccharomyces species through recent changes in noncoding sequence. Furthermore, these results show a clear example of how such background differences due to paralog divergence can drive changes in genome evolution.
| S-EPMC5308817 | biostudies-literature
Project description:Evolutionary divergence of Firre localization and expression
| PRJNA776631 | ENA
Project description:Gene duplication enables the emergence of new functions by lowering the general evolutionary pressure. Previous studies have highlighted the role of specific paralog genes during cell differentiation, e.g., in chromatin remodeling complexes. It remains unexplored whether similar mechanisms extend to other biological functions and whether the regulation of paralog genes is conserved across species. Here, we analyze the expression of paralogs across human tissues, during development and neuronal differentiation in fish, rodents and humans. While ~80% of paralog genes are co-regulated, a subset of paralogs shows divergent expression profiles, contributing to variability of protein complexes. We identify 78 substitutions of paralog pairs that occur during neuronal differentiation and are conserved across species. Among these, we highlight a substitution between the paralogs Sec23a and Sec23b subunits of the COPII complex. Altering the ratio between these two genes via RNAi-mediated knockdown is sufficient to influence the differentiation of immature neuron. We propose that remodeling of the vesicular transport system via paralog substitutions is an evolutionary conserved mechanism enabling neuronal differentiation.
2022-03-07 | PXD027387 | Pride
Project description:Gene duplication enables the emergence of new functions by lowering the general evolutionary pressure. Previous studies have highlighted the role of specific paralog genes during cell differentiation, e.g., in chromatin remodeling complexes. It remains unexplored whether similar mechanisms extend to other biological functions and whether the regulation of paralog genes is conserved across species. Here, we analyze the expression of paralogs across human tissues, during development and neuronal differentiation in fish, rodents and humans. While ~80% of paralog genes are co-regulated, a subset of paralogs shows divergent expression profiles, contributing to variability of protein complexes. We identify 78 substitutions of paralog eggNOG pairs that occur during neuronal differentiation and are conserved across species. Among these, we highlight a substitution between the paralogs Sec23a and Sec23b subunits of the COPII complex. Altering the ratio between these two genes via silencing-RNA knockdown was able to influence neuronal differentiation in different ways. We propose that remodeling of the vesicular transport system via paralog substitutions is an evolutionary conserved mechanism enabling neuronal differentiation.
2022-03-07 | PXD027191 | Pride
Project description:Gene duplication enables the emergence of new functions by lowering the general evolutionary pressure. Previous studies have highlighted the role of specific paralog genes during cell differentiation, e.g., in chromatin remodeling complexes. It remains unexplored whether similar mechanisms extend to other biological functions and whether the regulation of paralog genes is conserved across species. Here, we analyze the expression of paralogs across human tissues, during development and neuronal differentiation in fish, rodents and humans. While ~80% of paralog genes are co-regulated, a subset of paralogs shows divergent expression profiles, contributing to variability of protein complexes. We identify 78 substitutions of paralog eggNOG pairs that occur during neuronal differentiation and are conserved across species. Among these, we highlight a substitution between the paralogs Sec23a and Sec23b subunits of the COPII complex. Altering the ratio between these two genes via silencing-RNA knockdown was able to influence neuronal differentiation in different ways. We propose that remodeling of the vesicular transport system via paralog substitutions is an evolutionary conserved mechanism enabling neuronal differentiation.
2022-03-07 | PXD027195 | Pride
Project description:Throughout evolution, the duplication and functional divergence of transcription factors (TFs) has driven cellular and organismal complexity. Mechanisms by which paralogous TFs functionally diverge are thus of broad interest yet remain poorly understood. One well-established mechanism underlying TF divergence is the occupation and regulation of distinct sets of genes. Here we test for new mechanisms using CORONA (CNA) and PHABULOSA (PHB), two representative members of the CLASS III HOMEODOMAIN LEUCINE ZIPPER (HD-ZIPIII) family of plant TFs. CNA and PHB have largely overlapping binding profiles yet each paralog has hundreds of uniquely regulated targets. Regulation of a given gene thus depends on whether its local binding site is considered primed (inactive) or regulated (active) by CNA or PHB. This decision appears to be controlled, at least in part, by their lipid binding START domain, proposing a model in which HD-ZIPIII TFs use information integrated by their START domain to generate paralog-specific transcriptional outcomes at commonly bound genes. Taken together, our study identifies a new mechanism of TF paralog divergence and proposes the ubiquitously distributed START evolutionary module as a driver of functional divergence.
2024-10-08 | GSE253671 | GEO
Project description:Throughout evolution, the duplication and functional divergence of transcription factors (TFs) has driven cellular and organismal complexity. Mechanisms by which paralogous TFs functionally diverge are thus of broad interest yet remain poorly understood. One well-established mechanism underlying TF divergence is the occupation and regulation of distinct sets of genes. Here we test for new mechanisms using CORONA (CNA) and PHABULOSA (PHB), two representative members of the CLASS III HOMEODOMAIN LEUCINE ZIPPER (HD-ZIPIII) family of plant TFs. CNA and PHB have largely overlapping binding profiles yet each paralog has hundreds of uniquely regulated targets. Regulation of a given gene thus depends on whether its local binding site is considered primed (inactive) or regulated (active) by CNA or PHB. This decision appears to be controlled, at least in part, by their lipid binding START domain, proposing a model in which HD-ZIPIII TFs use information integrated by their START domain to generate paralog-specific transcriptional outcomes at commonly bound genes. Taken together, our study identifies a new mechanism of TF paralog divergence and proposes the ubiquitously distributed START evolutionary module as a driver of functional divergence.
2024-10-08 | GSE253674 | GEO
Project description:Reduction-oxidation (redox) signaling, the translation of an oxidative intracellular environment into a cellular response, is mediated by the reversible oxidation of specific cysteine thiols. The latter results in disulfide formation between protein (hetero)dimers that alter protein function until the cellular redox has returned to the basal state. We have previously shown that this mechanism promotes the nuclear localization and activity of the FOXO4 transcription factor. Here, we present evidence that FOXO3 and FOXO4 have acquired paralog-specific cysteines throughout vertebrate evolution. Using a proteome-wide screen we identified previously unknown redox-dependent FOXO3 interaction partners. The nuclear import receptor IPO7 forms a disulfide-dependent heterodimer with FOXO3, but not with FOXO4, which is required for reactive oxygen species (ROS)-induced nuclear translocation . These findings suggest that evolutionary acquisition of cysteines has contributed to functional divergence of FOXO paralogs.
2014-08-26 | PXD001040 | Pride