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Sayadi, Ahmed
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Publications (10 of 14) Show all publications
Stojkovic, B., Sayadi, A., Dordevic, M., Jovic, J., Savkovic, U. & Arnqvist, G. (2017). Divergent evolution of life span associated with mitochondrial DNA evolution. Evolution, 71(1), 160-166
Open this publication in new window or tab >>Divergent evolution of life span associated with mitochondrial DNA evolution
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2017 (English)In: Evolution, ISSN 0014-3820, E-ISSN 1558-5646, Vol. 71, no 1, p. 160-166Article in journal (Refereed) Published
Abstract [en]

Mitochondria play a key role in ageing. The pursuit of genes that regulate variation in life span and ageing have shown that several nuclear-encoded mitochondrial genes are important. However, the role of mitochondrial encoded genes (mtDNA) is more controversial and our appreciation of the role of mtDNA for the evolution of life span is limited. We use replicated lines of seed beetles that have been artificially selected for long or short life for >190 generations, now showing dramatic phenotypic differences, to test for a possible role of mtDNA in the divergent evolution of ageing and life span. We show that these divergent selection regimes led to the evolution of significantly different mtDNA haplotype frequencies. Selection for a long life and late reproduction generated positive selection for one specific haplotype, which was fixed in most such lines. In contrast, selection for reproduction early in life led to both positive selection as well as negative frequency-dependent selection on two different haplotypes, which were both present in all such lines. Our findings suggest that the evolution of life span was in part mediated by mtDNA, providing support for the emerging general tenet that adaptive evolution of life-history syndromes may involve mtDNA.

Place, publisher, year, edition, pages
WILEY-BLACKWELL, 2017
Keywords
Acanthoscelides obtectus, artificial selection, Bruchinae, coadaptation, mitochondria, mtDNA, negative frequency dependent selection, senescence
National Category
Genetics
Identifiers
urn:nbn:se:uu:diva-319809 (URN)10.1111/evo.13102 (DOI)000394439600014 ()27778315 (PubMedID)
Funder
EU, European Research Council, GENCON AdG-294333Swedish Research Council, 621-2010-5266
Available from: 2017-04-10 Created: 2017-04-10 Last updated: 2017-11-29Bibliographically approved
Immonen, E., Sayadi, A., Bayram, H. & Arnqvist, G. (2017). Mating Changes Sexually Dimorphic Gene Expression in the Seed Beetle Callosobruchus maculatus. Genome Biology and Evolution, 9(3), 677-699
Open this publication in new window or tab >>Mating Changes Sexually Dimorphic Gene Expression in the Seed Beetle Callosobruchus maculatus
2017 (English)In: Genome Biology and Evolution, ISSN 1759-6653, E-ISSN 1759-6653, Vol. 9, no 3, p. 677-699Article in journal (Refereed) Published
Abstract [en]

Sexually dimorphic phenotypes arise largely from sex-specific gene expression, which hasmainly been characterized in sexually naive adults. However, we expect sexual dimorphism in transcription to be dynamic and dependent on factors such as reproductive status. Mating induces many behavioral and physiological changes distinct to each sex and is therefore expected to activate regulatory changes in many sex-biased genes. Here, we first characterized sexual dimorphism in gene expression in Callosobruchus maculatus seed beetles. We then examined how females and males respond to mating and how it affects sex-biased expression, both in sex-limited (abdomen) and sex-shared (head and thorax) tissues. Mating responses were largely sex-specific and, as expected, females showed more genes responding compared with males (similar to 2,000 vs. similar to 300 genes in the abdomen, similar to 500 vs. similar to 400 in the head and thorax, respectively). Of the sex-biased genes present in virgins, 16%(1,041 genes) in the abdomen and 17%(243 genes) in the head and thorax altered their relative expression between the sexes as a result of mating. Sex-bias status changed in 2% of the genes in the abdomen and 4% in the head and thorax following mating. Mating responses involved de-feminization of females and, to a lesser extent, de-masculinization of males relative to their virgin state: mating decreased rather than increased dimorphic expression of sex-biased genes. The fact that regulatory changes of both types of sex-biased genes occurred in both sexes suggests that male-and female-specific selection is not restricted to male-and female-biased genes, respectively, as is sometimes assumed.

Keywords
RNA-Seq, transcriptome, sex-biased expression, sex-specific selection, alternative splicing
National Category
Genetics Evolutionary Biology
Identifiers
urn:nbn:se:uu:diva-326371 (URN)10.1093/gbe/evx029 (DOI)000402095700022 ()28391318 (PubMedID)
Funder
EU, European Research Council, AdG-294333Swedish Research Council, 621-2010-5266
Available from: 2017-07-07 Created: 2017-07-07 Last updated: 2018-08-10Bibliographically approved
Bayram, H. L., Sayadi, A., Goenaga, J., Immonen, E. & Arnqvist, G. (2017). Novel seminal fluid proteins in the seed beetle Callosobruchus maculatus identified by a proteomic and transcriptomic approach. Insect molecular biology (Print), 26(1), 58-73
Open this publication in new window or tab >>Novel seminal fluid proteins in the seed beetle Callosobruchus maculatus identified by a proteomic and transcriptomic approach
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2017 (English)In: Insect molecular biology (Print), ISSN 0962-1075, E-ISSN 1365-2583, Vol. 26, no 1, p. 58-73Article in journal (Refereed) Published
Abstract [en]

The seed beetle Callosobruchus maculatus is a significant agricultural pest and increasingly studied model of sexual conflict. Males possess genital spines that increase the transfer of seminal fluid proteins (SFPs) into the female body. As SFPs alter female behaviour and physiology, they are likely to modulate reproduction and sexual conflict in this species. Here, we identified SFPs using proteomics combined with a de novo transcriptome. A prior 2D-sodium dodecyl sulphate polyacrylamide gel electrophoresis analysis identified male accessory gland protein spots that were probably transferred to the female at mating. Proteomic analysis of these spots identified 98 proteins, a majority of which were also present within ejaculates collected from females. Standard annotation workflows revealed common functional groups for SFPs, including proteases and metabolic proteins. Transcriptomic analysis found 84 transcripts differentially expressed between the sexes. Notably, genes encoding 15 proteins were highly expressed in male abdomens and only negligibly expressed within females. Most of these sequences corresponded to 'unknown' proteins (nine of 15) and may represent rapidly evolving SFPs novel to seed beetles. Our combined analyses highlight 44 proteins for which there is strong evidence that they are SFPs. These results can inform further investigation, to better understand the molecular mechanisms of sexual conflict in seed beetles.

Keywords
evolution, reproduction, coleoptera, seminal fluid
National Category
Biochemistry and Molecular Biology
Identifiers
urn:nbn:se:uu:diva-315803 (URN)10.1111/imb.12271 (DOI)000391941200006 ()27779332 (PubMedID)
Funder
EU, European Research Council, GENCON AdG-294333Swedish Research Council, 621-2010-5266
Available from: 2017-02-22 Created: 2017-02-22 Last updated: 2018-08-10Bibliographically approved
Sayadi, A., Immonen, E., Tellgren-Roth, C. & Arnqvist, G. (2017). The Evolution of Dark Matter in the Mitogenome of Seed Beetles. Genome Biology and Evolution, 9(10), 2697-2706
Open this publication in new window or tab >>The Evolution of Dark Matter in the Mitogenome of Seed Beetles
2017 (English)In: Genome Biology and Evolution, ISSN 1759-6653, E-ISSN 1759-6653, Vol. 9, no 10, p. 2697-2706Article in journal (Refereed) Published
Abstract [en]

Animal mitogenomes are generally thought of as being economic and optimized for rapid replication and transcription. We use long-read sequencing technology to assemble the remarkable mitogenomes of four species of seed beetles. These are the largest circular mitogenomes ever assembled in insects, ranging from 24,496 to 26,613 bp in total length, and are exceptional in that some 40% consists of non-coding DNA. The size expansion is due to two very long intergenic spacers (LIGSs), rich in tandem repeats. The two LIGSs are present in all species but vary greatly in length (114-10,408 bp), show very low sequence similarity, divergent tandem repeat motifs, a very high AT content and concerted length evolution. The LIGSs have been retained for at least some 45 my but must have undergone repeated reductions and expansions, despite strong purifying selection on protein coding mtDNA genes. The LIGSs are located in two intergenic sites where a few recent studies of insects have also reported shorter LIGSs (>200 bp). These sites may represent spaces that tolerate neutral repeat array expansions or, alternatively, the LIGSs may function to allow a more economic translational machinery. Mitochondrial respiration in adult seed beetles is based almost exclusively on fatty acids, which reduces the need for building complex I of the oxidative phosphorylation pathway (NADH dehydrogenase). One possibility is thus that the LIGSs may allow depressed transcription of NAD genes. RNA sequencing showed that LIGSs are partly transcribed and transcriptional profiling suggested that all seven mtDNA NAD genes indeed show low levels of transcription and co-regulation of transcription across sexes and tissues.

Keywords
mitochondria, junk DNA, palindromes, Callosobruchus, Acanthoscelides, Bruchinae, intergenic spacers, metabolism, Coleoptera
National Category
Evolutionary Biology Genetics
Identifiers
urn:nbn:se:uu:diva-341670 (URN)10.1093/gbe/evx205 (DOI)000414778600018 ()29048527 (PubMedID)
Funder
EU, European Research Council, GENCON AdG-294333Swedish Research Council, 621-2014-4523
Available from: 2018-02-13 Created: 2018-02-13 Last updated: 2018-08-10Bibliographically approved
Arnqvist, G., Novicic, Z. K., Castro, J. A. & Sayadi, A. (2016). Negative frequency dependent selection on sympatric mtDNA haplotypes in Drosophila subobscura. Hereditas, 153, Article ID 15.
Open this publication in new window or tab >>Negative frequency dependent selection on sympatric mtDNA haplotypes in Drosophila subobscura
2016 (English)In: Hereditas, ISSN 0018-0661, E-ISSN 1601-5223, Vol. 153, article id 15Article in journal (Refereed) Published
Abstract [en]

Background: Recent experimental evidence for selection on mitochondrial DNA (mtDNA) has prompted the question as to what processes act to maintain within-population variation in mtDNA. Balancing selection though negative frequency dependent selection (NFDS) among sympatric haplotypes is a possibility, but direct empirical evidence for this is very scarce. Findings: We extend the previous findings of a multi-generation replicated cage experiment in Drosophila subobscura, where mtDNA polymorphism was maintained in a laboratory setting. First, we use a set of Monte Carlo simulations to show that the haplotype frequency dynamics observed are inconsistent with genetic drift alone and most closely match those expected under NFDS. Second, we show that haplotype frequency changes over time were significantly different from those expected under either genetic drift or positive selection but were consistent with those expected under NFSD. Conclusions: Collectively, our analyses provide novel support for NFDS on mtDNA haplotypes, suggesting that mtDNA polymorphism may at least in part be maintained by balancing selection also in natural populations. We very briefly discuss the possible mechanisms that might be involved.

Keywords
Balancing selection, mtDNA, Life history evolution, Polymorphism, Negative frequency dependent selection, SimuPop
National Category
Genetics
Identifiers
urn:nbn:se:uu:diva-315926 (URN)10.1186/s41065-016-0020-2 (DOI)000391695500001 ()28096777 (PubMedID)
Funder
EU, European Research Council, GENCON AdG-294333Swedish Research Council, 621-2014-4523
Available from: 2017-02-23 Created: 2017-02-23 Last updated: 2017-11-29Bibliographically approved
Sayadi, A., Jeyakani, J., Seet, S. H., Wei, C.-L., Bourque, G., Bard, F. A., . . . Bard-Chapeau, E. A. (2015). Functional features of EVI1 and EVI1Δ324 isoforms of MECOM gene in genome-wide transcription regulation and oncogenicity.. Oncogene
Open this publication in new window or tab >>Functional features of EVI1 and EVI1Δ324 isoforms of MECOM gene in genome-wide transcription regulation and oncogenicity.
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2015 (English)In: Oncogene, ISSN 0950-9232, E-ISSN 1476-5594Article in journal (Refereed) Epub ahead of print
Abstract [en]

The MDS1 and ecotropic viral integration site 1 (EVI1) complex locus (MECOM) gene encodes several transcription factor variants including MDS1-EVI1, EVI1 and EVI1Δ324. Although MDS1-EVI1 has been associated with tumor-suppressing activity, EVI1 is a known oncogene in various cancers, whose expression is associated with poor patient survival. Although EVI1Δ324 is co-transcribed with EVI1, its activity in cancer cells is not fully understood. Previous reports described that unlike EVI1, EVI1Δ324 protein cannot transform fibroblasts because of its disrupted N-terminal zinc finger (ZNF) domain. To better understand EVI1Δ324 biology and function, we obtained genome-wide binding occupancies and expression data in ovarian cancer cells. We characterized its DNA-binding sites, binding motif and target genes. Comparative analyses with previous study show that EVI1 and EVI1Δ324 share similar transcriptional activities linked to their common C-terminus ZNF domain. They bind to an E-twenty-six family (ETS)-like motif, target to a large extent the same genes and cooperate with AP1 transcription factor. EVI1Δ324-occupied genes were 70.7% similar to EVI1-bound genes. More strikingly, EVI1 and EVI1Δ324 differentially expressed genes were 99.87% identical, indicating comparable transcriptional regulatory functions. Consistently with gene ontologies linked to these target genes, EVI1Δ324 expression in HeLa cells could enhance anchorage-independent growth, such as EVI1, showing that EVI1Δ324 expression also lead to pro-oncogenic effects. The main specific feature of EVI1 variant is its N-terminus ZNF domain that binds DNA through GATA-like motif. We found that most GATA-like EVI1 chromatin immunoprecipitation sequencing peaks are far from genes and are not involved in transcriptional regulation. These genomic regions were enriched in simple sequence repeats and displayed high meiotic recombination rates. Overall, our genomics analyses uncovered common and specific features of two major MECOM isoforms. Their influence on transcription and downstream cell proliferation was comparable. However, EVI1-specific GATA-like binding sites, from its N-terminus ZNF domain, associated with high recombination rates, suggesting possible additional oncogenic potential for EVI1 in modulating genomic stability.Oncogene advance online publication, 3 August 2015; doi:10.1038/onc.2015.286.

National Category
Cancer and Oncology
Identifiers
urn:nbn:se:uu:diva-282516 (URN)10.1038/onc.2015.286 (DOI)26234679 (PubMedID)
Available from: 2016-04-05 Created: 2016-04-05 Last updated: 2017-11-30Bibliographically approved
Arnqvist, G., Sayadi, A., Immonen, E., Hotzy, C., Rankin, D., Tuda, M., . . . Johnston, J. S. (2015). Genome size correlates with reproductive fitness in seed beetles. Proceedings of the Royal Society of London. Biological Sciences, 282(1815), Article ID 20151421.
Open this publication in new window or tab >>Genome size correlates with reproductive fitness in seed beetles
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2015 (English)In: Proceedings of the Royal Society of London. Biological Sciences, ISSN 0962-8452, E-ISSN 1471-2954, Vol. 282, no 1815, article id 20151421Article in journal (Refereed) Published
Abstract [en]

The ultimate cause of genome size (GS) evolution in eukaryotes remains a major and unresolved puzzle in evolutionary biology. Large-scale comparative studies have failed to find consistent correlations between GS and organismal properties, resulting in the 'C-value paradox'. Current hypotheses for the evolution of GS are based either on the balance between mutational events and drift or on natural selection acting upon standing genetic variation in GS. It is, however, currently very difficult to evaluate the role of selection because within-species studies that relate variation in life-history traits to variation in GS are very rare. Here, we report phylogenetic comparative analyses of GS evolution in seed beetles at two distinct taxonomic scales, which combines replicated estimation of GS with experimental assays of life-history traits and reproductive fitness. GS showed rapid and bidirectional evolution across species, but did not show correlated evolution with any of several indices of the relative importance of genetic drift. Within a single species, GS varied by 4-5% across populations and showed positive correlated evolution with independent estimates of male and female reproductive fitness. Collectively, the phylogenetic pattern of GS diversification across and within species in conjunction with the pattern of correlated evolution between GS and fitness provide novel support for the tenet that natural selection plays a key role in shaping GS evolution.

Keywords
selfish DNA, Callosobruchus maculatus, population size, sexual dimorphism, sex chromosomes, sperm competition
National Category
Genetics Evolutionary Biology
Identifiers
urn:nbn:se:uu:diva-267333 (URN)10.1098/rspb.2015.1421 (DOI)000363357100013 ()
Funder
EU, European Research Council, AdG-294333Swedish Research Council, 621-2010-5266
Available from: 2015-11-24 Created: 2015-11-20 Last updated: 2018-08-10Bibliographically approved
Bard-Chapeau, E. A., Szumska, D., Jacob, B., Chua, B. Q., Chatterjee, G. C., Zhang, Y., . . . Copeland, N. G. (2014). Mice carrying a hypomorphic Evi1 allele are embryonic viable but exhibit severe congenital heart defects. PLoS ONE, 9(2)
Open this publication in new window or tab >>Mice carrying a hypomorphic Evi1 allele are embryonic viable but exhibit severe congenital heart defects
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2014 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 9, no 2Article in journal (Refereed) Published
Abstract [en]

The ecotropic viral integration site 1 (Evi1) oncogenic transcription factor is one of a number of alternative transcripts encoded by the Mds1 and Evi1 complex locus (Mecom). Overexpression of Evi1 has been observed in a number of myeloid disorders and is associated with poor patient survival. It is also amplified and/or overexpressed in many epithelial cancers including nasopharyngeal carcinoma, ovarian carcinoma, ependymomas, and lung and colorectal cancers. Two murine knockout models have also demonstrated Evi1's critical role in the maintenance of hematopoietic stem cell renewal with its absence resulting in the death of mutant embryos due to hematopoietic failure. Here we characterize a novel mouse model (designated Evi1(fl3)) in which Evi1 exon 3, which carries the ATG start, is flanked by loxP sites. Unexpectedly, we found that germline deletion of exon3 produces a hypomorphic allele due to the use of an alternative ATG start site located in exon 4, resulting in a minor Evi1 N-terminal truncation and a block in expression of the Mds1-Evi1 fusion transcript. Evi1(δex3/δex3) mutant embryos showed only a mild non-lethal hematopoietic phenotype and bone marrow failure was only observed in adult Vav-iCre/+, Evi1(fl3/fl3) mice in which exon 3 was specifically deleted in the hematopoietic system. Evi1(δex3/δex3) knockout pups are born in normal numbers but die during the perinatal period from congenital heart defects. Database searches identified 143 genes with similar mutant heart phenotypes as those observed in Evi1(δex3/δex3) mutant pups. Interestingly, 42 of these congenital heart defect genes contain known Evi1-binding sites, and expression of 18 of these genes are also effected by Evi1 siRNA knockdown. These results show a potential functional involvement of Evi1 target genes in heart development and indicate that Evi1 is part of a transcriptional program that regulates cardiac development in addition to the development of blood.

National Category
Cancer and Oncology
Identifiers
urn:nbn:se:uu:diva-282514 (URN)10.1371/journal.pone.0089397 (DOI)000332390800020 ()24586749 (PubMedID)
Available from: 2016-04-05 Created: 2016-04-05 Last updated: 2017-11-30Bibliographically approved
Bard-Chapeau, E. A., Nguyen, A.-T., Rust, A. G., Sayadi, A., Lee, P., Chua, B. Q., . . . Copeland, N. G. (2014). Transposon mutagenesis identifies genes driving hepatocellular carcinoma in a chronic hepatitis B mouse model.. Nature Genetics, 46(1)
Open this publication in new window or tab >>Transposon mutagenesis identifies genes driving hepatocellular carcinoma in a chronic hepatitis B mouse model.
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2014 (English)In: Nature Genetics, ISSN 1061-4036, E-ISSN 1546-1718, Vol. 46, no 1Article in journal (Refereed) Published
Abstract [en]

The most common risk factor for developing hepatocellular carcinoma (HCC) is chronic infection with hepatitis B virus (HBV). To better understand the evolutionary forces driving HCC, we performed a near-saturating transposon mutagenesis screen in a mouse HBV model of HCC. This screen identified 21 candidate early stage drivers and a very large number (2,860) of candidate later stage drivers that were enriched for genes that are mutated, deregulated or functioning in signaling pathways important for human HCC, with a striking 1,199 genes being linked to cellular metabolic processes. Our study provides a comprehensive overview of the genetic landscape of HCC.

National Category
Cancer and Oncology
Identifiers
urn:nbn:se:uu:diva-282513 (URN)10.1038/ng.2847 (DOI)24316982 (PubMedID)
Available from: 2016-04-05 Created: 2016-04-05 Last updated: 2017-11-30Bibliographically approved
Dudgeon, C., Shreeram, S., Tanoue, K., Mazur, S. J., Sayadi, A., Robinson, R. C., . . . Bulavin, D. V. (2013). Genetic variants and mutations of PPM1D control the response to DNA damage. Cell Cycle, 12(16)
Open this publication in new window or tab >>Genetic variants and mutations of PPM1D control the response to DNA damage
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2013 (English)In: Cell Cycle, ISSN 1538-4101, E-ISSN 1551-4005, Vol. 12, no 16Article in journal (Refereed) Published
Abstract [en]

The Wip1 phosphatase is an oncogene that is overexpressed in a variety of primary human cancers. We were interested in identifying genetic variants that could change Wip1 activity. We identified 3 missense SNPs of the human Wip1 phosphatase, L120F, P322Q, and I496V confer a dominant-negative phenotype. On the other hand, in primary human cancers, PPM1D mutations commonly result in a gain-of-function phenotype, leading us to identify a hot-spot truncating mutation at position 525. Surprisingly, we also found a significant number of loss-of-function mutations of PPM1D in primary human cancers, both in the phosphatase domain and in the C terminus. Thus, PPM1D has evolved to generate genetic variants with lower activity, potentially providing a better fitness for the organism through suppression of multiple diseases. In cancer, however, the situation is more complex, and the presence of both activating and inhibiting mutations requires further investigation to understand their contribution to tumorigenesis.

National Category
Genetics
Identifiers
urn:nbn:se:uu:diva-282512 (URN)10.4161/cc.25694 (DOI)23907125 (PubMedID)
Available from: 2016-04-05 Created: 2016-04-05 Last updated: 2017-11-30Bibliographically approved
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