
Group photo of Tom Cooper, M.D., and his lab members.
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About the Lab

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.
Cooper Lab News
Dr. Larissa Nitschke has been awarded a two-year postdoctoral fellowship award from the Myotonic Dystrophy Foundation beginning in 2022.
Matt Penna was selected for a travel award to attend the 2021 Frontiers in Myogenesis Conference in Costa Rica.
Matt Penna was awarded an NIH F31 Predoctoral Award.
Ashish Rao defended his thesis in June 2021.
Sara Johnson’s paper was accepted by Wiley Interdiscip Reviews RNA.
Ashish Rao’s paper describing our DM1 heart mouse model accepted for publication in JCI Insight.
Rong-Chi Hu was awarded a two-year predoctoral fellowship from the Myotonic Dystrophy Foundation starting January 2021 through December 2022.
Reagents
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
Alternative splicing is crucial to muscle mass maintenance
Alternative splicing allows cells to make many different proteins with a limited number of genes.
There is more going on in DM1 than just alternative splicing
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.
What causes myotonic dystrophy, type1
The lab of Dr. Thomas Cooper discovered that the CUGexp RNA disrupts the regulation of RNA splicing that is important for proper functions of a large number of genes.
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