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Tuck, Simon
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Publications (10 of 37) Show all publications
Nilsson, L., Rahmani, S. & Tuck, S. (2021). C. elegans TAT-6, a putative aminophospholipid translocase, is expressed in sujc cells in the hermaphrodite gonad. microPublication biology
Open this publication in new window or tab >>C. elegans TAT-6, a putative aminophospholipid translocase, is expressed in sujc cells in the hermaphrodite gonad
2021 (English)In: microPublication biology, ISSN 2578-9430Article in journal (Refereed) Published
Abstract [en]

In healthy eukaryotic cells, the two leaflets that make up plasma membranes are highly asymmetric with respect to the lipids they contain. In both unicellular eukaryotes and metazoans, the asymmetry in the distribution of aminophospholipids is maintained by P4-family transmembrane ATPases, which catalyze the movement of selected phospholipids from the outer leaflet to the inner. C. elegans has six P4-family ATPases, TAT-1 - TAT-6. TAT-1 - TAT-5 are expressed in many tissues and cells. Here we report that, in contrast, TAT-6 is much less broadly expressed and that, within the somatic gonad, expression of TAT-6 reporters is restricted to the spermathecal-uterine core cell (sujc) cells.

Place, publisher, year, edition, pages
Caltech Library, 2021
National Category
Biochemistry and Molecular Biology Cell Biology
Identifiers
urn:nbn:se:umu:diva-191136 (URN)10.17912/micropub.biology.000495 (DOI)34746684 (PubMedID)
Note

Published 2021-04-11

Available from: 2022-01-10 Created: 2022-01-10 Last updated: 2022-01-11Bibliographically approved
Rahmani, S. & Tuck, S. (2021). EGL-4 promotes turning behavior of C. elegans males during mating. microPublication biology
Open this publication in new window or tab >>EGL-4 promotes turning behavior of C. elegans males during mating
2021 (English)In: microPublication biology, ISSN 2578-9430Article in journal (Refereed) Published
Abstract [en]

During mating, C. elegans males whose tails have reached the head or tail of their intended mates are able to switch to scanning the other side by performing a turn during which the male's tail curls ventrally all the while keeping in contact with the hermaphrodite. The ability to execute turns efficiently is dependent upon serotonergic neurons in the posterior ventral nerve cord that stimulate diagonal muscles by activating a serotonin receptor, SER-1. Here we show that turning behavior is abnormal in males lacking a cGMP-dependent protein kinase, EGL-4. egl-4 mutant males are also resistant to ventral tail curling induced by exogenous serotonin.

Place, publisher, year, edition, pages
Caltech Library, 2021
National Category
Ecology Evolutionary Biology Zoology
Identifiers
urn:nbn:se:umu:diva-191134 (URN)10.17912/micropub.biology.000433 (DOI)34423280 (PubMedID)
Note

Published 2021-08-18

Available from: 2022-01-10 Created: 2022-01-10 Last updated: 2022-01-11Bibliographically approved
Herdenberg, C., Mutie, P., Billing, O., Abdullah, A., Strawbridge, R. J., Dahlman, I., . . . Hedman, H. (2021). LRIG proteins regulate lipid metabolism via BMP signaling and affect the risk of type 2 diabetes. Communications Biology, 4(1), Article ID 90.
Open this publication in new window or tab >>LRIG proteins regulate lipid metabolism via BMP signaling and affect the risk of type 2 diabetes
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2021 (English)In: Communications Biology, E-ISSN 2399-3642, Vol. 4, no 1, article id 90Article in journal (Refereed) Published
Abstract [en]

Leucine-rich repeats and immunoglobulin-like domains (LRIG) proteins have been implicated as regulators of growth factor signaling; however, the possible redundancy among mammalian LRIG1, LRIG2, and LRIG3 has hindered detailed elucidation of their physiological functions. Here, we show that Lrig-null mouse embryonic fibroblasts (MEFs) are deficient in adipogenesis and bone morphogenetic protein (BMP) signaling. In contrast, transforming growth factor-beta (TGF-beta) and receptor tyrosine kinase (RTK) signaling appeared unaltered in Lrig-null cells. The BMP signaling defect was rescued by ectopic expression of LRIG1 or LRIG3 but not by expression of LRIG2. Caenorhabditis elegans with mutant LRIG/sma-10 variants also exhibited a lipid storage defect. Human LRIG1 variants were strongly associated with increased body mass index (BMI) yet protected against type 2 diabetes; these effects were likely mediated by altered adipocyte morphology. These results demonstrate that LRIG proteins function as evolutionarily conserved regulators of lipid metabolism and BMP signaling and have implications for human disease. Herdenberg et al. show that adipogenesis and BMP signaling are altered in mouse cells deficient in LRIG (Leucine-rich repeats and immunoglobulin-like domains) proteins. They find that mutant LRIG/sma-10 variant worms exhibit lipid storage defects and that human LRIG1 variants are associated with higher body mass index, yet protect against type 2 diabetes. This study suggests an evolutionarily conserved role of LRIG proteins for lipid metabolism and BMP signaling.

Place, publisher, year, edition, pages
Springer Nature, 2021
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:umu:diva-180823 (URN)10.1038/s42003-020-01613-w (DOI)000613509200014 ()33469151 (PubMedID)2-s2.0-85099541477 (Scopus ID)
Available from: 2021-02-26 Created: 2021-02-26 Last updated: 2024-07-02Bibliographically approved
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)2-s2.0-85062975493 (Scopus ID)
Available from: 2019-08-12 Created: 2019-08-12 Last updated: 2023-03-24Bibliographically 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, E-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)2-s2.0-85068116757 (Scopus ID)
Available from: 2019-01-22 Created: 2019-01-22 Last updated: 2023-03-23Bibliographically 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)2-s2.0-85026669140 (Scopus ID)
Available from: 2017-09-06 Created: 2017-09-06 Last updated: 2023-03-24Bibliographically 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: 2024-07-02Bibliographically 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, 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)2-s2.0-84927650804 (Scopus ID)
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: 2023-03-23Bibliographically 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 ()2-s2.0-84892557625 (Scopus ID)
Available from: 2014-04-07 Created: 2014-03-18 Last updated: 2023-03-24Bibliographically approved
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