Difference between revisions of "Dionne"

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==Welcome to the Dionne lab!==
  
Welcome to the Dionne lab!
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That is to say, Marc Dionne's lab, at King's College London; not to be confused with any other Dionne lab.
  
We are interested in (1) the effects of host genetics on the biology of infection; and (2) the physiological control of metabolic balance. We use the fruitfly ''Drosophila melanogaster'' as a model organism to study these questions; this allows us to screen for genes that affect these processes in a rapid and unbiased fashion.
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We are interested in (1) the effects of host genetics on the biology of infection; and (2) cytokine signalling and its effects on immune and non-immune tissues. ''Drosophila melanogaster'' is our animal model of choice.
  
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Work in the lab is funded by [http://www.bbsrc.ac.uk the Biotechnology and Biological Sciences Research Council] and [http://www.wellcome.ac.uk the Wellcome Trust].
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==We've moved!==
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The lab has moved from its original digs (on the 27th and 28th floors of Guy's Tower) across the street to New Hunt's House in order to be part of the new Centre for the Molecular and Cellular Biology of Inflammation. Our academic affiliation will be changing to the Peter Gorer Department of Immunobiology, DIIID, School of Medicine. Directions and postal addresses have been corrected on the [http://dionne.openwetware.org/Contact.html Contact] page.
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==Host genetics and the biology of infection==
 +
 +
Different individuals show different levels of resistance to infections and develop different pathologies in response to infections. We are interested in why this is the case.  We use the fruitfly ''Drosophila melanogaster'' as a model host to study these questions; this allows us to screen for genes that affect the progress of infection in a rapid and unbiased fashion.
 +
 +
All of our experiments originate from a simple genetic screen. Mutant flies are infected with ''Mycobacterium marinum'', a bacterium closely-related to the causative agent of tuberculosis, or with ''Mycobacterium smegmatis'', a related non-pathogen. We select lines of flies that die more quickly or more slowly than wild-type controls and identify the mutation that gives rise to this phenotype. We then try to understand what this phenotype tells us about the function of the mutated gene.
 +
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So far, our work on this system has focused on the mechanisms of pathogenesis. We have found that this infection causes progressive loss of metabolic stores, similar to the wasting seen in people with tuberculosis. We have shown that, in the fly, this wasting effect is caused partly by systemic failures in anabolic signals via the insulin effector kinase Akt. We are now working to try to understand how infection causes this defect in anabolic signalling. We also have mutants that affect other aspects of disease; we are working with these mutants to understand  other aspects of disease pathogenesis as well as how the fly immune system fights Mycobacterial infections.
 +
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==Cytokines and cytokine signalling==
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 +
In the course of screening, we find a lot of molecules and pathways that end up being involved in cytokine signalling and its consequences. One aspect of this is the metabolic effects of infection, which appear to result from high levels of cytokine expression over several days. Cytokines also regulate the realized immune response of the fly, much as they do in mammals.
 +
 +
We've recently published some of this work in "Current Biology", showing that two different TGF-betas regulate fly immunity, each inhibiting a specific arm of the immune response, and each being produced by only a subset of phagocytes. [http://www.ncbi.nlm.nih.gov/pubmed/21962711 Check it out!]
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==Recent updates to the lab wiki==
 
==Recent updates to the lab wiki==
 
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Revision as of 12:27, 12 November 2011

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About Us       Protocols &c.       Lab Members       Publications       Contact       Links


Welcome to the Dionne lab!

That is to say, Marc Dionne's lab, at King's College London; not to be confused with any other Dionne lab.

We are interested in (1) the effects of host genetics on the biology of infection; and (2) cytokine signalling and its effects on immune and non-immune tissues. Drosophila melanogaster is our animal model of choice.

Work in the lab is funded by the Biotechnology and Biological Sciences Research Council and the Wellcome Trust.

We've moved!

The lab has moved from its original digs (on the 27th and 28th floors of Guy's Tower) across the street to New Hunt's House in order to be part of the new Centre for the Molecular and Cellular Biology of Inflammation. Our academic affiliation will be changing to the Peter Gorer Department of Immunobiology, DIIID, School of Medicine. Directions and postal addresses have been corrected on the Contact page.

Host genetics and the biology of infection

Different individuals show different levels of resistance to infections and develop different pathologies in response to infections. We are interested in why this is the case. We use the fruitfly Drosophila melanogaster as a model host to study these questions; this allows us to screen for genes that affect the progress of infection in a rapid and unbiased fashion.

All of our experiments originate from a simple genetic screen. Mutant flies are infected with Mycobacterium marinum, a bacterium closely-related to the causative agent of tuberculosis, or with Mycobacterium smegmatis, a related non-pathogen. We select lines of flies that die more quickly or more slowly than wild-type controls and identify the mutation that gives rise to this phenotype. We then try to understand what this phenotype tells us about the function of the mutated gene.

So far, our work on this system has focused on the mechanisms of pathogenesis. We have found that this infection causes progressive loss of metabolic stores, similar to the wasting seen in people with tuberculosis. We have shown that, in the fly, this wasting effect is caused partly by systemic failures in anabolic signals via the insulin effector kinase Akt. We are now working to try to understand how infection causes this defect in anabolic signalling. We also have mutants that affect other aspects of disease; we are working with these mutants to understand other aspects of disease pathogenesis as well as how the fly immune system fights Mycobacterial infections.

Cytokines and cytokine signalling

In the course of screening, we find a lot of molecules and pathways that end up being involved in cytokine signalling and its consequences. One aspect of this is the metabolic effects of infection, which appear to result from high levels of cytokine expression over several days. Cytokines also regulate the realized immune response of the fly, much as they do in mammals.

We've recently published some of this work in "Current Biology", showing that two different TGF-betas regulate fly immunity, each inhibiting a specific arm of the immune response, and each being produced by only a subset of phagocytes. Check it out!

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Recent updates to the lab wiki

20 October 2017

     09:23  Carrico‎ (diff | hist) . . (-305). . Yar (talk | contribs) (use mediawiki markup for images, not raw html)
     09:15 (User creation log) . . User account Msupestka (talk | contribs) was created by Yar (talk | contribs) and password was sent by email ‎

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Beauchamp:DataSharing‎‎ (2 changes | history) . . (+228). . [John Magnotti‎ (2×)]

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     08:02  Peyton: Lab Meeting Schedule Fall 2017‎ (diff | hist) . . (0). . Maria F. Gencoglu (talk | contribs)
     07:49  Min-Ho Kim Lab:Lab Members‎ (diff | hist) . . (-89). . Min-Ho Kim (talk | contribs)

19 October 2017

     21:07  BME100 f2017:Group7 W0800 L4‎ (diff | hist) . . (+977). . Miguel R. Almanza Lopez (talk | contribs) (SNP Information & Primer Design)

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BME100 f2017:Group6 W1030 L4‎‎ (4 changes | history) . . (+1,447). . [Ray Gerard Regorgo‎ (4×)]

     

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(cur | prev) . . (-196). . Ray Gerard Regorgo (talk | contribs) (OUR TEAM)

     

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     15:43  User:Julie A. Fogarty‎ (diff | hist) . . (+46). . Julie A. Fogarty (talk | contribs) (Julie A. Fogarty)

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Rich Lab:Funding‎‎ (2 changes | history) . . (-12). . [Isabel C. Morales‎ (2×)]

     

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(cur | prev) . . (+685). . Peteral (talk | contribs) (Week 2: Me Myself and I-dentifiers, The Key To Immortality (Persistence))

     

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(cur | prev) . . (+319). . Weinjule (talk | contribs) (Papers)

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User:Peteral‎‎ (3 changes | history) . . (+1,264). . [Peteral‎ (3×)]

     

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BME100 f2017:Group14 W0800 L4‎‎ (9 changes | history) . . (+9). . [Shae M. Diaz‎ (9×)]

     

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(cur | prev) . . (+8). . Shae M. Diaz (talk | contribs) (Protocol)

     

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(cur | prev) . . (-31). . Shae M. Diaz (talk | contribs) (TEAM MEMBERS)

     

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 m   14:12  Swartz‎ (diff | hist) . . (+61). . Marcus Rohovie (talk | contribs)
     14:10 (Move log) . . Marcus Rohovie (talk | contribs) moved page Swartz to Swartz:Main

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(Upload log). .

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Klenow Assembly Method: Seamless cloning‎‎ (3 changes | history) . . (+101). . [David M.D. Bailey‎ (3×)]

     

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(cur | prev) . . (-5). . David M.D. Bailey (talk | contribs) (The Klenow Assembly Method (KAM) for the seamless cloning of overlapping double stranded DNA fragments: Very cheap alternative to the Gibson Assembly)

     

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(cur | prev) . . (+1). . David M.D. Bailey (talk | contribs) (The Klenow Assembly Method (KAM) for the seamless cloning of overlapping double stranded DNA fragments: Very cheap alternative to the Gibson Assembly)

     

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