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.
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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.
  
We are interested in (1) the effects of host genetics on the biology of infection; and (2) the physiological control of metabolic balance.
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Work in the lab has been funded by [http://www.bbsrc.ac.uk the Biotechnology and Biological Sciences Research Council] and [http://www.wellcome.ac.uk the Wellcome Trust].
  
 
==Host genetics and the biology of infection==
 
==Host genetics and the biology of infection==
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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.
 
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 determine 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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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 how the fly immune system fights Mycobacterial infections as well as other aspects of disease pathogenesis.
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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, broadly 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 Akt and the TOR effector p70 S6 kinase.
  
==Physiological control of metabolic balance==
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Most recently, we have shown that the transcription factor MEF2 responds to nutrient signals to regulate expression of both immune effectors and anabolic enzymes. Remarkably, though MEF2 promotes the expression of both groups of genes, its choice of targets is regulated by a conserved phosphorylation that alters its affinity for the TATA binding protein. [http://www.cell.com/abstract/S0092-8674(13)01144-6 This work has recently been published in ''Cell''.]
  
As mentioned above, we've found that infection with ''M marinum'' causes serious metabolic defects in ''Drosophila''. At least some of these effects are due to changes in signalling pathways whose roles in metabolic control are largely unexplored or completely unknown. This has led us to examine the roles of these pathways in metabolic control in healthy animals so that we can then understand the effects of infection-induced perturbation of these pathways.
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==Cytokines and cytokine signalling==
  
This work is preliminary but is very exciting - we hope to be able to say more soon!
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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.
  
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Some time back, we 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.cell.com/current-biology/abstract/S0960-9822(11)00954-7 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 06:03, 28 September 2013

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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 has been funded by the Biotechnology and Biological Sciences Research Council and the Wellcome Trust.

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, broadly 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 Akt and the TOR effector p70 S6 kinase.

Most recently, we have shown that the transcription factor MEF2 responds to nutrient signals to regulate expression of both immune effectors and anabolic enzymes. Remarkably, though MEF2 promotes the expression of both groups of genes, its choice of targets is regulated by a conserved phosphorylation that alters its affinity for the TATA binding protein. This work has recently been published in Cell.

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.

Some time back, we 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

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21 October 2020

     23:59  BIOL368/F20:Class Journal Week 7‎‎ 20 changes history +29,993 [Taylor Makela‎; Macie Duran‎; Jcorrey‎; Nidapatel‎ (2×); Nathan R. Beshai‎ (2×); Kam Taghizadeh‎ (2×); Falghane‎ (2×); BallonaBuddy‎ (4×); Aiden Burnett‎ (5×)]
     
23:59 (cur | prev) +3,396 Taylor Makela talk contribs Added Taylor Makela
     
22:56 (cur | prev) +105 Kam Taghizadeh talk contribs added talk
     
22:55 (cur | prev) +1,131 Kam Taghizadeh talk contribs added answers
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22:54 (cur | prev) 0 Nidapatel talk contribs Nida Patel journal entry
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22:53 (cur | prev) +3,349 Nidapatel talk contribs Nida Patel journal entry
     
22:33 (cur | prev) +5,833 Jcorrey talk contribs added my responses - JT
     
21:34 (cur | prev) +99 BallonaBuddy talk contribs signing
     
21:17 (cur | prev) +3,388 BallonaBuddy talk contribs finishing class journal assignment
     
20:38 (cur | prev) +154 BallonaBuddy talk contribs title and third question
     
19:34 (cur | prev) +4,504 Macie Duran talk contribs Macie Duran added response
     
19:22 (cur | prev) +366 Nathan R. Beshai talk contribs added Dr. Speicher question
     
19:17 (cur | prev) +2,110 Nathan R. Beshai talk contribs Added post reading questions
     
19:09 (cur | prev) +223 Aiden Burnett talk contribs →‎Aiden Burnett: finished
     
18:56 (cur | prev) +1,322 BallonaBuddy talk contribs comment on workshop and relevance in career
     
18:48 (cur | prev) +245 Aiden Burnett talk contribs →‎After you do the readings: wrote text
     
18:45 (cur | prev) +312 Aiden Burnett talk contribs →‎Aiden Burnett: wrote text
     
18:41 (cur | prev) +610 Aiden Burnett talk contribs →‎Aiden Burnett: wrote text
     
18:30 (cur | prev) +456 Aiden Burnett talk contribs →‎Aiden Burnett: wrote answer 1
     
17:59 (cur | prev) +213 Falghane talk contribs →‎In preparation for Dr. Stephen Speicher's visit next week: fatimah added
     
17:53 (cur | prev) +2,177 Falghane talk contribs fatimah added questions and answers
     23:35  Taylor Makela Journal Week 7‎‎ 2 changes history +1,346 [Taylor Makela‎ (2×)]
     
23:35 (cur | prev) -13 Taylor Makela talk contribs removed extra template header
     
23:35 (cur | prev) +1,359 Taylor Makela talk contribs added acknowledgments, references, and template
     23:02  Kam Taghizadeh Week 7‎‎ 3 changes history +2,031 [Kam Taghizadeh‎ (3×)]
     
23:02 (cur | prev) +1,229 Kam Taghizadeh talk contribs added references
     
23:01 (cur | prev) -20 Kam Taghizadeh talk contribs deleted header
     
23:00 (cur | prev) +822 Kam Taghizadeh talk contribs added acknowledgements
N    23:02  Nida Patel Journal Week 7‎‎ 2 changes history +1,252 [Nidapatel‎ (2×)]
     
23:02 (cur | prev) +820 Nidapatel talk contribs →‎Acknowledgements: template added
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23:01 (cur | prev) +432 Nidapatel talk contribs acknowledgements section added
N    22:38  JT Correy Journal Week 7 diffhist +1,668 Jcorrey talk contribs made page
N    21:36  Ian R. Wright Week 7‎‎ 5 changes history +972 [BallonaBuddy‎ (5×)]
     
21:36 (cur | prev) +276 BallonaBuddy talk contribs acknowledgements
     
21:33 (cur | prev) +53 BallonaBuddy talk contribs acknowledgements
     
21:32 (cur | prev) +442 BallonaBuddy talk contribs references
     
18:58 (cur | prev) +138 BallonaBuddy talk contribs adding bodenreider reference
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18:44 (cur | prev) +63 BallonaBuddy talk contribs invoking template and starting references and acknowledgements
     19:15  Aiden Burnett Week 7‎‎ 3 changes history +1,253 [Aiden Burnett‎ (3×)]
     
19:15 (cur | prev) +111 Aiden Burnett talk contribs →‎Acknowledgments: last acknowledgment (easy week huh Annika)
     
19:12 (cur | prev) +815 Aiden Burnett talk contribs →‎References: wrote references
     
19:11 (cur | prev) +327 Aiden Burnett talk contribs →‎Acknowledgments: wrote ackn
     18:52  Renhao Li Lab:Lab Members‎‎ 3 changes history +350 [Renhao Li‎ (3×)]
     
18:52 (cur | prev) +307 Renhao Li talk contribs →‎Alumni
     
18:45 (cur | prev) +71 Renhao Li talk contribs →‎Alumni
     
18:41 (cur | prev) -28 Renhao Li talk contribs →‎Current Members
     18:50  Yaniv Maddahi Journal Week 7‎‎ 2 changes history +223 [Yaniv Maddahi‎ (2×)]
     
18:50 (cur | prev) +1 Yaniv Maddahi talk contribs →‎References: fixed week
     
18:50 (cur | prev) +222 Yaniv Maddahi talk contribs →‎Acknowledgements: added phrase
     18:02  BIOL368/S19 Week 7 diffhist +206 Falghane talk contribs signature added
     18:01  Template:Falghane BIO368 diffhist +215 Falghane talk contribs Individual journal name added
     17:16  BIOL368/F20:Week 8‎‎ 5 changes history +489 [Kam D. Dahlquist‎ (5×)]
     
17:16 (cur | prev) +260 Kam D. Dahlquist talk contribs →‎Read: add second article
     
17:14 (cur | prev) +216 Kam D. Dahlquist talk contribs →‎Shared Journal Assignment: change direction, add new reading
     
17:06 (cur | prev) +13 Kam D. Dahlquist talk contribs →‎Database Evaluation: uncomment last question and clarify about partners
     
17:04 (cur | prev) -52 Kam D. Dahlquist talk contribs →‎Database Evaluation: delete redundant sentence
     
17:04 (cur | prev) +52 Kam D. Dahlquist talk contribs →‎Database Evaluation: bold/italics one hyperlink per answer
     17:13  Macie Duran Week 7‎‎ 2 changes history +1,572 [Macie Duran‎ (2×)]
     
17:13 (cur | prev) +800 Macie Duran talk contribs →‎Acknowledgments: added acknowledgments
     
17:04 (cur | prev) +772 Macie Duran talk contribs →‎References: added references

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