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Tuck, Simon
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Publications (10 of 30) Show all publications
Rohn, I., Raschke, S., Aschner, M., Tuck, S., Kuehnelt, D., Kipp, A., . . . Bornhorst, J. (2019). Treatment of Caenorhabditis elegans with Small Selenium Species Enhances Antioxidant Defense Systems. Molecular Nutrition & Food Research, 63(9)
Open this publication in new window or tab >>Treatment of Caenorhabditis elegans with Small Selenium Species Enhances Antioxidant Defense Systems
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2019 (English)In: Molecular Nutrition & Food Research, ISSN 1613-4125, E-ISSN 1613-4133, Vol. 63, no 9Article in journal (Refereed) Published
Abstract [en]

ScopeSmall selenium (Se) species play a key role in Se metabolism and act as dietary sources of the essential trace element. However, they are redox-active and trigger pro- and antioxidant responses. As health outcomes are strongly species-dependent, species-specific characteristics of Se compounds are tested in vivo. Methods and resultsIn the model organism Caenorhabditis elegans (C. elegans), immediate and sustained effects of selenite, selenomethionine (SeMet), and Se-methylselenocysteine (MeSeCys) are studied regarding their bioavailability, incorporation into proteins, as well as modulation of the cellular redox status. While all tested Se compounds are bioavailable, only SeMet persistently accumulates and is non-specifically incorporated into proteins. However, the protection toward chemically-induced formation of reactive species is independent of the applied Se compound. Increased thioredoxin reductase (TXNRD) activity and changes in mRNA expression levels of antioxidant proteins indicate the activation of cellular defense mechanisms. However, in txnrd-1 deletion mutants, no protective effects of the Se species are observed anymore, which is also reflected by differential gene expression data. ConclusionSe species protect against chemically-induced reactive species formation. The identified immediate and sustained systemic effects of Se species give rise to speculations on possible benefits facing subsequent periods of inadequate Se intake.

Place, publisher, year, edition, pages
WILEY, 2019
Keywords
antioxidant defense systems, caenorhabditis elegans, selenium, oxidative stress, selenoproteins
National Category
Biochemistry and Molecular Biology
Identifiers
urn:nbn:se:umu:diva-162022 (URN)10.1002/mnfr.201801304 (DOI)000476955800008 ()30815971 (PubMedID)
Available from: 2019-08-12 Created: 2019-08-12 Last updated: 2019-08-12Bibliographically approved
Dongre, M., Singh, B., Aung, K. M., Larsson, P., Miftakhova, R. R., Persson, K., . . . Wai, S. N. (2018). Flagella-mediated secretion of a novel Vibrio cholerae cytotoxin affecting both vertebrate and invertebrate hosts. Communications Biology, 1, Article ID 59.
Open this publication in new window or tab >>Flagella-mediated secretion of a novel Vibrio cholerae cytotoxin affecting both vertebrate and invertebrate hosts
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2018 (English)In: Communications Biology, ISSN 2399-3642, Vol. 1, article id 59Article in journal (Refereed) Published
Abstract [en]

Using Caenorhabditis elegans as an infection host model for Vibrio cholerae predator interactions, we discovered a bacterial cytotoxin, MakA, whose function as a virulence factor relies on secretion via the flagellum channel in a proton motive force-dependent manner. The MakA protein is expressed from the polycistronic makDCBA (motility-associated killing factor) operon. Bacteria expressing makDCBA induced dramatic changes in intestinal morphology leading to a defecation defect, starvation and death in C. elegans. The Mak proteins also promoted V. cholerae colonization of the zebrafish gut causing lethal infection. A structural model of purified MakA at 1.9 Å resolution indicated similarities to members of a superfamily of bacterial toxins with unknown biological roles. Our findings reveal an unrecognized role for V. cholerae flagella in cytotoxin export that may contribute both to environmental spread of the bacteria by promoting survival and proliferation in encounters with predators, and to pathophysiological effects during infections.

Place, publisher, year, edition, pages
Springer Nature Publishing AG, 2018
National Category
Microbiology in the medical area
Research subject
Infectious Diseases; Molecular Biology
Identifiers
urn:nbn:se:umu:diva-155563 (URN)10.1038/s42003-018-0065-z (DOI)000461126500059 ()30271941 (PubMedID)
Available from: 2019-01-22 Created: 2019-01-22 Last updated: 2019-04-04Bibliographically approved
Rohn, I., Marschall, T. A., Kroepfl, N., Jensen, K. B., Aschner, M., Tuck, S., . . . Bornhorst, J. (2018). Selenium species-dependent toxicity, bioavailability and metabolic transformations in Caenorhabditis elegans. Metallomics, 10(6), 818-827
Open this publication in new window or tab >>Selenium species-dependent toxicity, bioavailability and metabolic transformations in Caenorhabditis elegans
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2018 (English)In: Metallomics, ISSN 1756-5901, E-ISSN 1756-591X, Vol. 10, no 6, p. 818-827Article in journal (Refereed) Published
Abstract [en]

The essential micronutrient selenium (Se) is required for various systemic functions, but its beneficial range is narrow and overexposure may result in adverse health effects. Additionally, the chemical form of the ingested selenium contributes crucially to its health effects. While small Se species play a major role in Se metabolism, their toxicological effects, bioavailability and metabolic transformations following elevated uptake are poorly understood. Utilizing the tractable invertebrate Caenorhabditis elegans allowed for an alternative approach to study species-specific characteristics of organic and inorganic Se forms in vivo, revealing remarkable species-dependent differences in the toxicity and bioavailability of selenite, selenomethionine (SeMet) and Se-methylselenocysteine (MeSeCys). An inverse relationship was found between toxicity and bioavailability of the Se species, with the organic species displaying a higher bioavailability than the inorganic form, yet being less toxic. Quantitative Se speciation analysis with HPLC/mass spectrometry revealed a partial metabolism of SeMet and MeSeCys. In SeMet exposed worms, identified metabolites were Se-adenosylselenomethionine (AdoSeMet) and Se-adenosylselenohomocysteine (AdoSeHcy), while worms exposed to MeSeCys produced Se-methylselenoglutathione (MeSeGSH) and -glutamyl-MeSeCys (-Glu-MeSeCys). Moreover, the possible role of the sole selenoprotein in the nematode, thioredoxin reductase-1 (TrxR-1), was studied comparing wildtype and trxr-1 deletion mutants. Although a lower basal Se level was detected in trxr-1 mutants, Se toxicity and bioavailability following acute exposure was indistinguishable from wildtype worms. Altogether, the current study demonstrates the suitability of C. elegans as a model for Se species dependent toxicity and metabolism, while further research is needed to elucidate TrxR-1 function in the nematode.

Place, publisher, year, edition, pages
Royal Society of Chemistry, 2018
National Category
Biochemistry and Molecular Biology
Identifiers
urn:nbn:se:umu:diva-150875 (URN)10.1039/c8mt00066b (DOI)000436031100004 ()29770420 (PubMedID)2-s2.0-85048929897 (Scopus ID)
Available from: 2018-08-31 Created: 2018-08-31 Last updated: 2018-08-31Bibliographically approved
Navarro-Gonzalez, C., Moukadiri, I., Villarroya, M., Lopez-Pascual, E., Tuck, S. & Eugenia Armengod, M. (2017). Mutations in the Caenorhabditis elegans orthologs of human genes required for mitochondrial tRNA modification cause similar electron transport chain defects but different nuclear responses. PLoS Genetics, 13(7), Article ID e1006921.
Open this publication in new window or tab >>Mutations in the Caenorhabditis elegans orthologs of human genes required for mitochondrial tRNA modification cause similar electron transport chain defects but different nuclear responses
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2017 (English)In: PLoS Genetics, ISSN 1553-7390, E-ISSN 1553-7404, Vol. 13, no 7, article id e1006921Article in journal (Refereed) Published
Abstract [en]

Several oxidative phosphorylation (OXPHOS) diseases are caused by defects in the post-transcriptional modification of mitochondrial tRNAs (mt-tRNAs). Mutations in MTO1 or GTPBP3 impair the modification of the wobble uridine at position 5 of the pyrimidine ring and cause heart failure. Mutations in TRMU affect modification at position 2 and cause liver disease. Presently, the molecular basis of the diseases and why mutations in the different genes lead to such different clinical symptoms is poorly understood. Here we use Caenorhabditis elegans as a model organism to investigate how defects in the TRMU, GTPBP3 and MTO1 orthologues (designated as mttu-1, mtcu-1, and mtcu-2, respectively) exert their effects. We found that whereas the inactivation of each C. elegans gene is associated with a mild OXPHOS dysfunction, mutations in mtcu-1 or mtcu-2 cause changes in the expression of metabolic and mitochondrial stress response genes that are quite different from those caused by mttu-1 mutations. Our data suggest that retrograde signaling promotes defect-specific metabolic reprogramming, which is able to rescue the OXPHOS dysfunction in the single mutants by stimulating the oxidative tricarboxylic acid cycle flux through complex II. This adaptive response, however, appears to be associated with a biological cost since the single mutant worms exhibit thermosensitivity and decreased fertility and, in the case of mttu-1, longer reproductive cycle. Notably, mttu-1 worms also exhibit increased lifespan. We further show that mtcu-1; mttu-1 and mtcu-2; mttu-1 double mutants display severe growth defects and sterility. The animal models presented here support the idea that the pathological states in humans may initially develop not as a direct consequence of a bioenergetic defect, but from the cell's maladaptive response to the hypomodification status of mt-tRNAs. Our work highlights the important association of the defect-specific metabolic rewiring with the pathological phenotype, which must be taken into consideration in exploring specific therapeutic interventions.

National Category
Medical Genetics
Identifiers
urn:nbn:se:umu:diva-139017 (URN)10.1371/journal.pgen.1006921 (DOI)000406615300051 ()28732077 (PubMedID)
Available from: 2017-09-06 Created: 2017-09-06 Last updated: 2018-06-09Bibliographically approved
Sheng, M., Gorzsás, A. & Tuck, S. (2016). Fourier transform infrared microspectroscopy for the analysis of the biochemical composition of C. elegans worms. Worm, 5(1), Article ID e1132978.
Open this publication in new window or tab >>Fourier transform infrared microspectroscopy for the analysis of the biochemical composition of C. elegans worms
2016 (English)In: Worm, E-ISSN 2162-4054, Vol. 5, no 1, article id e1132978Article in journal (Refereed) Published
Abstract [en]

Changes in intermediary metabolism have profound effects on many aspects of C. elegans biology including growth, development and behavior. However, many traditional biochemical techniques for analyzing chemical composition require relatively large amounts of starting material precluding the analysis of mutants that cannot be grown in large amounts as homozygotes. Here we describe a technique for detecting changes in the chemical compositions of C. elegans worms by Fourier transform infrared microspectroscopy. We demonstrate that the technique can be used to detect changes in the relative levels of carbohydrates, proteins and lipids in one and the same worm. We suggest that Fourier transform infrared microspectroscopy represents a useful addition to the arsenal of techniques for metabolic studies of C. elegans worms.

Place, publisher, year, edition, pages
Taylor & Francis, 2016
Keywords
C. elegans, carbohydrate, composition, Fourier transform infrared, lipid, microspectroscopy, protein
National Category
Biochemistry and Molecular Biology
Identifiers
urn:nbn:se:umu:diva-111049 (URN)10.1080/21624054.2015.1132978 (DOI)27073735 (PubMedID)
Note

Originally included in thesis in manuscript form, with the title "Fourier transform infrared microspectroscopy for the analysis of the biochemical composition of C. elegans".

Available from: 2015-11-02 Created: 2015-11-02 Last updated: 2018-06-07Bibliographically approved
Sheng, M., Hosseinzadeh, A., Muralidharan, S. V., Gaur, R., Selstam, E. & Tuck, S. (2015). Aberrant Fat Metabolism in Caenorhabditis elegans Mutants with Defects in the Defecation Motor Program. PLoS ONE, 10(4), Article ID e0124515.
Open this publication in new window or tab >>Aberrant Fat Metabolism in Caenorhabditis elegans Mutants with Defects in the Defecation Motor Program
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2015 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 10, no 4, article id e0124515Article in journal (Refereed) Published
Abstract [en]

The molecular mechanisms by which dietary fatty acids are absorbed by the intestine, and the way in which the process is regulated are poorly understood. In a genetic screen for mutations affecting fat accumulation in the intestine of Caenorhabditis elegans, nematode worms, we have isolated mutations in the aex-5 gene, which encodes a Kex2/subtilisinfamily, Ca2+-sensitive proprotein convertase known to be required for maturation of certain neuropeptides, and for a discrete step in an ultradian rhythmic phenomenon called the defecation motor program. We demonstrate that aex-5 mutants have markedly lower steadystate levels of fat in the intestine, and that this defect is associated with a significant reduction in the rate at which labeled fatty acid derivatives are taken up from the intestinal lumen. Other mutations affecting the defecation motor program also affect steady-state levels of triglycerides, suggesting that the program is required per se for the proper accumulation of neutral lipids. Our results suggest that an important function of the defecation motor program in C. elegans is to promote the uptake of an important class of dietary nutrients. They also imply that modulation of the program might be one way in which worms adjust nutrient uptake in response to altered metabolic status.

Place, publisher, year, edition, pages
PLOS one, 2015
National Category
Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:umu:diva-103146 (URN)10.1371/journal.pone.0124515 (DOI)000352477800268 ()25849533 (PubMedID)
Funder
Swedish Cancer Society, 12 0534
Note

supported by grants from Vetenskapsrådet (K2012-67X-20441-063) and Cancerfonden (12 0534).

Available from: 2015-05-29 Created: 2015-05-18 Last updated: 2018-06-07Bibliographically approved
Tuck, S. (2014). The control of cell growth and body size in Caenorhabditis elegans. Experimental Cell Research, 321(1), 71-76
Open this publication in new window or tab >>The control of cell growth and body size in Caenorhabditis elegans
2014 (English)In: Experimental Cell Research, ISSN 0014-4827, E-ISSN 1090-2422, Vol. 321, no 1, p. 71-76Article, review/survey (Refereed) Published
Abstract [en]

One of the most important ways in which animal species vary is in their size. Individuals of the largest animal ever thought to have lived, the blue whale (Balaenoptera musculus), can reach a weight of 190 t and a length of over 30 m. At the other extreme, among the smallest multicellular animals are males of the parasitic wasp, Dicopomorpha echmepterygis, which even as adults are just 140 mu m in length. In terms of volume, these species differ by more than 14 orders of magnitude. Since size has such profound effects on an organism's ecology, anatomy and physiology, an important task for evolutionary biology and ecology is to account for why organisms grow to their characteristic sizes. Equally, a full description of an organism's development must include an explanation of how its growth and body size are regulated. Here I review research on how these processes are controlled in the nematode, Caenorhabditis elegans. Analyses of small and long mutants have revealed that in the worm, DBL-1, a ligand in the TGF beta superfamily family, promotes growth in a dose-dependent manner. DBL-1 signaling affects body size by stimulating the growth of syncytial hypodermal cells rather than controlling cell division. Signals from chemosensory neurons and from the gonad also modulate body size, in part, independently of DBL-1-mediated signaling. Organismal size and morphology is heavily influenced by the cuticle, which acts as the exoskeleton. Finally, I summarize research on several genes that appear to regulate body size by cell autonomously regulating cell growth throughout the worm. 

Keywords
Caenorhabditis elegans, Body size, TGFbeta, dbl-1, BMP
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-87037 (URN)10.1016/j.yexcr.2013.11.007 (DOI)000331157200011 ()
Available from: 2014-04-07 Created: 2014-03-18 Last updated: 2018-06-08Bibliographically approved
Korta, D. Z., Tuck, S. & Hubbard, E. J. (2012). S6K links cell fate, cell cycle and nutrient response in C. elegans germline stem/progenitor cells.. Development, 139(5), 859-870
Open this publication in new window or tab >>S6K links cell fate, cell cycle and nutrient response in C. elegans germline stem/progenitor cells.
2012 (English)In: Development, ISSN 0950-1991, E-ISSN 1477-9129, Vol. 139, no 5, p. 859-870Article in journal (Refereed) Published
Abstract [en]

Coupling of stem/progenitor cell proliferation and differentiation to organismal physiological demands ensures the proper growth and homeostasis of tissues. However, in vivo mechanisms underlying this control are poorly characterized. We investigated the role of ribosomal protein S6 kinase (S6K) at the intersection of nutrition and the establishment of a stem/progenitor cell population using the C. elegans germ line as a model. We find that rsks-1 (which encodes the worm homolog of mammalian p70S6K) is required germline-autonomously for proper establishment of the germline progenitor pool. In the germ line, rsks-1 promotes cell cycle progression and inhibits larval progenitor differentiation, promotes growth of adult tumors and requires a conserved TOR phosphorylation site. Loss of rsks-1 and ife-1 (eIF4E) together reduces the germline progenitor pool more severely than either single mutant and similarly to reducing the activity of let-363 (TOR) or daf-15 (RAPTOR). Moreover, rsks-1 acts in parallel with the glp-1 (Notch) and daf-2 (insulin-IGF receptor) pathways, and does not share the same genetic dependencies with its role in lifespan control. We show that overall dietary restriction and amino acid deprivation cause germline defects similar to a subset of rsks-1 mutant phenotypes. Consistent with a link between diet and germline proliferation via rsks-1, loss of rsks-1 renders the germ line largely insensitive to the effects of dietary restriction. Our studies establish the C. elegans germ line as an in vivo model to understand TOR-S6K signaling in proliferation and differentiation and suggest that this pathway is a key nutrient-responsive regulator of germline progenitors.

National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:umu:diva-52803 (URN)10.1242/dev.074047 (DOI)22278922 (PubMedID)
Available from: 2012-03-02 Created: 2012-03-02 Last updated: 2018-06-08Bibliographically approved
Nilsson, L., Jonsson, E. & Tuck, S. (2011). Caenorhabditis elegans Numb Inhibits Endocytic Recycling by Binding TAT-1 Aminophospholipid Translocase. Traffic: the International Journal of Intracellular Transport, 12(12), 1839-1849
Open this publication in new window or tab >>Caenorhabditis elegans Numb Inhibits Endocytic Recycling by Binding TAT-1 Aminophospholipid Translocase
2011 (English)In: Traffic: the International Journal of Intracellular Transport, ISSN 1398-9219, E-ISSN 1600-0854, Vol. 12, no 12, p. 1839-1849Article in journal (Refereed) Published
Abstract [en]

Numb regulates endocytosis in many metazoans, but the mechanism by which it functions is not completely understood. Here we report that the Caenorhabditis ele-gans Numb ortholog, NUM-1A, a regulator of endocytic recycling, binds the C isoform of transbilayer amphipath transporter-1 (TAT-1), a P4 family adenosine triphosphatase and putative aminophospholipid translocase that is required for proper endocytic trafficking. We demonstrate that TAT-1 is differentially spliced during development and that TAT-1C-specific splicing occurs in the intestine where NUM-1A is known to function. NUM-1A and TAT-1C colocalize in vivo. We have mapped the binding site to an NXXF motif in TAT-1C. This motif is not required for TAT-1C function but is required for NUM-1A's ability to inhibit recycling. We demonstrate that num-1A and tat-1 defects are both suppressed by the loss of the activity of PSSY-1, a phosphatidylserine (PS) synthase. PS is mislocalized in intestinal cells with defects in tat-1 or num-1A function. We propose that NUM-1A inhibits recycling by inhibiting TAT-1C's ability to translocate PS across the membranes of recycling endosomes.

Place, publisher, year, edition, pages
Malden: Wiley-Blackwell, 2011
Keywords
C. elegans, endocytosis, numb, phosphatidylserine, recycling, tat-1
National Category
Cell Biology
Identifiers
urn:nbn:se:umu:diva-50937 (URN)10.1111/j.1600-0854.2011.01271.x (DOI)000297573500014 ()21917090 (PubMedID)
Available from: 2012-01-05 Created: 2012-01-02 Last updated: 2018-06-08Bibliographically approved
Tuck, S. (2011). Extracellular vesicles: budding regulated by a phosphatidylethanolamine translocase. Current Biology, 21(24), R988-R990
Open this publication in new window or tab >>Extracellular vesicles: budding regulated by a phosphatidylethanolamine translocase
2011 (English)In: Current Biology, ISSN 0960-9822, E-ISSN 1879-0445, Vol. 21, no 24, p. R988-R990Article in journal (Refereed) Published
Abstract [en]

Recent work on a Caenorhabditis elegans transmembrane ATPase reveals a central role for the aminophospholipid phosphatidylethanolamine in the production of a class of extracellular vesicles

Keywords
biological-membranes; bleeding disorder; scott-syndrome; protein; flippases; mechanism; tmem16f
National Category
Cell and Molecular Biology Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy)
Identifiers
urn:nbn:se:umu:diva-51467 (URN)10.1016/j.cub.2011.11.009 (DOI)000298440100009 ()
Available from: 2012-01-24 Created: 2012-01-23 Last updated: 2018-06-08Bibliographically approved
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