Tom Cooper Lab

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Tom Cooper Lab group photo 2019
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About Us

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Research at The Cooper Lab.
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The realization that most human genes generate multiple mRNAs encoding divergent protein isoforms via alternative splicing and polyadenylation has revealed extensive regulation that remains to be explored.

Alternative pathways of RNA processing are regulated in response to signaling cues often coordinating expression of gene networks in response to physiological change including in development and disease.

We are interested in understanding the mechanisms and consequences of this regulation, from how RNA binding proteins and signaling pathways coordinate RNA processing networks to the functional consequences of the different protein isoforms that are expressed in different cell states.

We also investigate the pathogenic mechanisms of myotonic dystrophy, type 1 (DM1), an autosomal dominant neuromuscular disorder affecting multiple tissues including muscle, heart and the central nervous system. The pathogenic mechanism is disruption of developmentally regulated RNA processing, primarily alternative splicing, in which failure to express adult splicing patterns causes primary features of the disease.

The understanding of the molecular mechanisms of DM1 pathogenesis has led to development of several therapeutic approaches some of which are being testing using mouse models established in the lab.

These investigations utilize a combination of cell culture and genetic models including transgenic and knock out mouse lines for RNA binding proteins, CRISPR-derived mouse lines in which specific alternative exons are removed, and DM1 mouse models.

The overlapping areas of investigation in the lab lead to synergistic and collaborative interactions in which knowledge gained in one area fosters progress in the others.

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Cooper Lab News

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Diana¹s abstract was selected for a platform presentation at the Eukaryotic mRNA Processing Meeting at Cold Spring Harbor August 2019.

Abstracts submitted by Diana, Paul, Ashish were selected for talks award at the biannual IDMC12 meeting in Gothenburg, Sweden and Paul won award for best talk.

Ashish Rao was awarded a two-year predoctoral fellowship from the Myotonic Dystrophy Foundation starting January 2018 through December 2020.

Paul Pang was awarded a three-year predoctoral F31 NRSA fellowship from the NIH to start in 2018 through 2021. 

Diana Cox was awarded a three-year predoctoral F31 NRSA fellowship from the NIH to starting in 2018 through 2021.

Paul won best poster award at the 2019 IMBS graduate program annual retreat.

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Reagents

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The following plasmids are available through Addgene.

FRE5 (FLAGNLSREDGFP5)
FRE5Cf (FLAGNLSREDGFP5Claf)
RG6
RHCglo
RTB300
R300TA
DT960
DT480
DT240
DT40
DT12A
DT0
pBItetDT960GFP
pBItetDT12nGFP
FLYLQ (Flag-CELF1)
pBItetDMPKSGFP
pBItetDT240GFP
pBItetDT480GFP
FlagETR3 (CELF2)
FlagMBNL1-41
FlagMBNL3

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National Human Genome Research Institute
Alternative splicing allows cells to make many different proteins with a limited number of genes.
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Alternative splicing is crucial to muscle mass maintenance

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Alternative splicing allows cells to make many different proteins with a limited number of genes.

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National Human Genome Research Institute/Ernesto del Aguila III
Mouse models of human genetic conditions are valuable tools to better understand and potentially treat human diseases.
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There is more going on in DM1 than just alternative splicing

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In his laboratory at Baylor College of Medicine, Dr. Thomas A. Cooper is leading the way to better understand myotonic dystrophy type 1 (DM1), a rare but devastating condition.