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Dahan, O.

Publications and source records attributed to Dahan, O..

10 recordsLinked to original sources

Evolution of a genome-architecture-encoded gene regulation system in trypanosomatids

Transcriptional regulation of protein-coding genes is a hallmark of eukaryotic gene expression. Yet, a group of parasitic protists, trypanosomatids, appear to lack this capability. Here, we analyzed genomic, nascent transcriptomic, RNA polymerase occupancy and gene organization data to reconstruct the evolutionary origin and biological consequences of their unusual regulatory strategy. Across 59 Discoba protists, we show stepwise evolutionary erosion of conventional transcription regulation components in trypanosomatida lineage, including gene consolidation into polycistronic transcription units (PTUs), shortening of intra-PTU non-coding regions, and depletion of transcription factors and their enriched DNA-binding motifs. This transition was associated with near-constitutive expression of most genes, indicating broad loss of conditional gene expression. However, trypanosomatids retain some differential regulation at the PTU level, with >70% PTUs featuring significantly different nascent transcription than their neighbors or resident chromosomes. Moreover, gene expression is not uniform within PTUs: nascent transcription, translation efficiency, and protein abundance progressively decline with distance from the transcription start site. Consistent with this architecture-encoded regulatory logic, co-complex subunits and co-pathway enzymes preferentially occupy adjacent positions within PTUs despite each PTUs overall functional heterogeneity. These findings reveal an evolutionary shift from gene-specific transcriptional regulation toward a regime where genome architecture becomes a regulator of gene expression.

evolutionary biology↗

The evolutionary origin of host association and polycistronic transcription in trypanosomatids

Trypanosomatids (Kinetoplastids) encompass multiple lineages of parasitic protists with monoxenous or dixenous life cycles, infecting insects, vertebrates, and plants; in vertebrate hosts, some are intracellular, while others are extracellular. To understand the origin and diversification of their host associations, we integrated comparative genomics across 47 genomes. Results highlight that monoxenous, extracellular trypanosomatids originated from predatory ancestors through reductive evolution, which diminished their metabolic and hunting capabilities. Intracellularity and dixenous lifestyle convergently originated three times independently. Progressive consolidation of genes into polycistronic transcription units (PTUs) was a central innovation that began in early Glycomonada and expanded through chromosome fission-fusion and gene relocation/inversion. In present-day PTUs, protein complex subunits and metabolic pathway enzymes are positioned for co-expression in temporal synchrony, and chromosomes minimize colinear PTUs to counter transcriptional readthrough. Together, these results provide a time-resolved origin of host-association and polycistronic transcription in trypanosomatids, possibly through an intermediate phase of facultative parasitism.

evolutionary biology↗

Encoded and non-genetic alternative protein variants expand human functional proteome

Each stage of the Central Dogma contributes to proteome diversity through mechanisms such as heterozygosity, somatic mutations, transcriptional errors, and translational errors. As a result, a diverse array of protein variants can coexist within a single proteome, such as that of humans. However, until now, methods to detect, quantify, and evaluate the functional consequences of these variants have been lacking. Here we examined a large-scale proteogenomic dataset from 29 healthy human tissues and uncovered 13,910 confidently localized variants representing 7,215 unique single amino acid substitutions co-existing alongside their corresponding reference proteoforms. We found that the abundance of both genetic (SNPs, somatic mutations) and mistranslated protein variants mirrors their allele frequencies in the human population. Moreover, we show that non-genetic substitutions may provide a distinct route for exploring protein sequence space, circumventing the mutational constraints imposed by the genetic code. In addition, we provide experimental validation of non-genetic substitution on selected purified proteins. We demonstrate specific and recurring non-genetic variation patterns upon amino acid starvation in proteome-wide analyses of cancer-derived cell lines and identify hundreds of substituted non-genetic proteoforms that recur consistently in multiple healthy individuals or map to annotated protein functional sites. We propose that these substitutions constitute a novel class of functional protein phenotypic variants. Collectively, our findings indicate that non-genetic amino acid substitutions in human proteins provide an abundant source to expanding the functional proteome.

molecular biology↗

Essentiality and dynamic expression of the human tRNA pool during viral infection

Human viruses depend on the translation resources of the host cell. A significant translation resource is the tRNA pool of the cell, as human viruses do not encode tRNA genes. Through tRNA sequencing, we inspected the human tRNA pool upon infection of human Cytomegalovirus (HCMV) and SARS-CoV-2. HCMV-induced alterations in tRNA expression were predominantly virus-driven, with minimal influence from the cellular immune response. Notably, specific tRNA post-transcriptional modifications appeared to modulate stability and were susceptible to HCMV manipulation. In contrast, SARS-CoV-2 infection did not significantly impact tRNA expression or modifications. We compared the codon usage of viral genes to the proliferation-differentiation codon-usage signatures of human genes. We found a marked difference between the viruses, with HCMV genes aligning with differentiation codon usage and SARS-CoV-2 genes reflecting proliferation codon usage. We further found that codon usage of structural and gene expression-related viral genes displayed high adaptation to host cell tRNA pools. Through a systematic CRISPR screen targeting human tRNA genes and modification enzymes, we identified specific tRNAs and enzymes that improve or reduce HCMV infectivity and cellular growth. These findings highlight the dynamic interplay between the tRNA pool and viral infection dynamics, shedding light on mechanisms governing host-virus interactions.

genomics↗

Adaptive Mate Selection in Saccharomyces cerevisiae Revealed Through a High-Throughput Mating Assay

In evolutionary biology, sexual mating plays a pivotal role in facilitating the combination of beneficial alleles among individuals. Cross-species data suggest that organisms selectively mate with partners based on factors such as genetic distance and partner fitness. Understanding the determinants of pair-specific mating affinity is crucial for unraveling the impact of sex on evolution. However, despite the significance of this phenomenon, the availability of large and consistent datasets is limited, leading to inconsistent conclusions. To address this gap, we present a comprehensive mating assay enabling the simultaneous quantification of mating affinity among approximately 100 natural Saccharomyces cerevisiae strains. Our study demonstrates that mating in an en masse manner, allowing mating based on affinity, enhances the overall fitness of the hybrids offspring population compared to mating that enforces one specific partner at a time. By employing a DNA barcode recombination system integrated into natural isolates genomes, we sequence recombined barcode pairs and revealed mating frequencies and affinities among all strains in different environments. Our findings unveil strain-specific mating affinity among natural yeast strains, with certain parental pairs exhibiting a heightened affinity for each other over other strains, whereas certain strains combinations are avoided. Notably, among the pairs with the highest affinity, there is a preference for lower genetic distances. Intriguingly, multiple strains show a propensity for mating with partners that yield higher-fitness hybrids on average. Collectively, our results provide compelling evidence that yeast actively engages in adaptive mate affinity.

evolutionary biology↗

Quantitative genetics of natural S. cerevisiae strains upon sexual mating reveals heritable determinants of cellular fitness

Quantitative genetics requires large datasets of diverse phenotyped-genotyped strains from the same species. A special need is for such archived biological material and computerized data in sexually reproducing individuals from a species. Here we leverage sexual mating among close to 100 diverse natural isolates of the yeast S. cerevisiae that form about 4,000 hybrids combinations in several ecologically relevant growth conditions. In a first genetic study of this new resource we focus on fitness measurements and its modes of inheritance as a quantitative trait from parents to offspring hybrids. We employ genomic barcoding of all strains and a barcode recombination technique to follow hybrids of each successful mate combination. For all parents, and separately for all offspring hybrids we measure fitness under each condition. We focus on the inheritance of fitness, the ultimate evolutionary trait, and its inheritance as a quantitative trait upon sexual mating. Predicting hybrid fitness given parental parameters is a major challenge as it is likely multi-factorial. We find that hybrids fitness in fermentable carbon source correlates positively, yet modestly, with parental fitness, while on non-fermentable carbon, hybrid fitness shows no detectable correlation with parental fitness. Instead, the non-fermentable condition, hybrid fitness increases sharply with genetic distance between their parents, suggesting that outbreeding maximizes fitness irrespective of parental fitness at that condition. The number of minor alleles in the genome of each hybrid, analogous to polygenic risk score in classical genetics, negatively correlates with fitness in both conditions. Fitness inheritance can be explained by either a dominance or a co-dominance modes of inheritance, in the non-fermentable and fermentable conditions respectively. Our newly suggested biological resource and data provide new foundations for a quantitative research in genetics and evolution upon sexual mating. Furthermore, our barcoded strains and mating tracking method provide an important research resource for the yeast community.

genetics↗

Manipulation of the human tRNA pool reveals distinct tRNA sets that act in cellular proliferation or cell cycle arrest

Different subsets of the tRNA pool in human are expressed in different cellular conditions. The "proliferation-tRNAs" are induced upon normal and cancerous cell division, while the "differentiation tRNAs" are active in non-dividing, differentiated cells. Here we examine the essentiality of the various tRNAs upon cellular growth and arrest. We established a CRISPR-based editing procedure with sgRNAs that each target a tRNA family. We measured tRNA essentiality for cellular growth and found that most proliferation tRNAs are essential compared to differentiation tRNAs in rapidly growing cell lines. Yet in more slowly dividing lines, the differentiation tRNAs were more essential. In addition, we measured these tRNAs roles upon response to cell cycle arresting signals. Here we detected a more complex behavior with both proliferation-tRNAs and differentiation tRNAs showing various levels of essentiality. These results provide the so-far most comprehensive functional characterization of human tRNAs with intricate roles in various proliferation states.

molecular biology↗

Sequence determinants and evolution of splicing in budding yeast and related species

RNA splicing is a key process in eukaryotic gene expression. Most Intron-containing genes are constitutively spliced, hence efficient splicing of an intron is crucial for efficient gene expression. Here we use a large synthetic oligo library of ~20,000 variants to explore how different intronic sequence features affect splicing efficiency and mRNA expression levels in S. cerevisiae. Using a combinatorial design of synthetic introns we demonstrate how non-consensus splice site sequences affect splicing efficiency in each of the three splice sites. We then show that S. cerevisiae splicing machinery tends to select alternative 3 splice sites downstream of the original site, and we suggest that this tendency created a selective pressure, leading to the avoidance of cryptic splice site motifs near introns 3 ends. We further use natural intronic sequences from other yeast species, whose splicing machineries have diverged to various extents, to show how intron architectures in the various species have been adapted to the organisms splicing machinery. We suggest that the observed tendency for cryptic splicing is a result of a loss of a specific splicing factor, U2AF1. Lastly, we show that synthetic sequences containing two introns give rise to alternative RNA isoforms in S. cerevisiae, exposing intronic features that control and facilitate alternative splicing. Our study reveals novel mechanisms by which introns are shaped in evolution to allow cells to regulate their transcriptome.

systems biology↗

Dynamic changes in tRNA modifications and abundance during T-cell activation

The tRNA pool determines the efficiency, throughput, and accuracy of translation. Previous studies have identified dynamic changes in the tRNA supply and mRNA demand during cancerous proliferation. Yet, dynamic changes may occur also during physiologically normal proliferation, and these are less characterized. We examined the tRNA and mRNA pools of T-cells during their vigorous proliferation and differentiation upon triggering their antigen receptor. We observe a global signature of switch in demand for codons at the early proliferation phase of the response, accompanied by corresponding changes in tRNA expression levels. In the later phase, upon differentiation, the response of the tRNA pool is relaxed back to basal level, potentially restraining excessive proliferation. Sequencing of tRNAs allowed us to also evaluate their diverse base-modifications. We found that two types of tRNA modifications, wybutosine and ms2t6A, are reduced dramatically during T-cell activation. These modifications occur in the anti-codon loops of two tRNAs that decode "slippery codons", that are prone to ribosomal frameshifting. Attenuation of these frameshift-protective modifications is expected to increase the potential for proteome-wide frameshifting during T-cell proliferation. Indeed, human cell lines deleted of a wybutosine writer showed increased ribosomal frameshifting, as detected with a HIV gag-pol frameshifting site reporter. These results may explain HIVs specific tropism towards proliferating T-Cells since it requires ribosomal frameshift exactly on the corresponding codon for infection. The changes in tRNA expression and modifications uncover a new layer of translation regulation during T-cell proliferation and exposes a potential trade-off between cellular growth and translation fidelity. Significance statementThe tRNA pool decodes genetic information during translation. As such, it is subject to intricate physiological regulation in all species, across different physiological conditions. Here we show for the first time a program that governs the tRNA pool and its interaction with the transcriptome upon a physiological cellular proliferation- T-cells activation. We found that upon antigenic activation of T-cells, their tRNA and mRNA pools undergo coordinated and complementary changes, which are relaxed when cells reduce back their proliferation rate and differentiate into memory cells. We found a reduction in two particular tRNA modifications that have a role in governing translation fidelity and frameshift prevention. This exposes a vulnerability in activated T-cells that may be utilized by HIV for its replication. ClassificationBIOLOGICAL SCIENCES; cell biology

genomics↗

Systematic detection of amino acid substitutions in proteome reveals a mechanistic basis of ribosome errors

Translation errors limit the accuracy of information transmission from DNA to proteins. Selective pressures shape the way cells produce their proteins: the translation machinery and the mRNA sequences it decodes co-evolved to ensure that translation proceeds fast and accurately in a wide range of environmental conditions. Our understanding of the causes of amino acid misincorporations and of their effect on the evolution of protein sequences is largely hindered by the lack of experimental methods to observe errors at the full proteome level. Here, we systematically detect and quantify errors in entire proteomes from mass spectrometry data. Following HPLC MS-MS data acquisition, we identify E. coli and S. cerevisiae peptides whose mass and fragment ion spectrum are consistent with that of a peptide bearing a single amino acid substitution, and verify that such spectrum cannot result from a post-translational modification. Our analyses confirm that most substitutions occur due to codon-to-anticodon mispairing within the ribosome. Patterns of errors due to mispairing were similar in bacteria and yeast, suggesting that the error spectrum is chemically constrained. Treating E. coli cells with a drug known to affect ribosomal proofreading increased the error rates due to mispairing at the wobble codon position. Starving bacteria for serine resulted in specific patterns of substitutions reflecting the amino acid deficiency. Overall, translation errors tend to occur at positions that are less evolutionarily conserved, and that minimally affect protein energetic stability, indicating that they are selected against. Genome wide ribosome density data suggest that errors occur at sites where ribosome velocity is relatively high, supporting the notion of a trade-off between speed and accuracy as predicted by proofreading theories. Together our results reveal a mechanistic basis for ribosome errors in translation.

systems biology↗