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We are recruiting postdocs and graduate students for new and ongoing projects.
- Graduate Students
- Postdoctoral Associates
Graduate Students:
- Contact Tom Cooper to discuss rotation opportunities.
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
Larissa’s perspective of a paper from the John Lueck lab was published in J. Clinical Investigation
Lathan’s review of microtubules in skeletal muscle development and homeostasis published in Int J Mol Sci. 2023 10.3390/ijms24032903
Larissa was awarded a three year NIH F32 postdoctoral fellowship award to start January 2024
Sara’s abstract was selected for an oral presentation at the 2023 Eukaryotic mRNA Processing meeting
Janel’s abstract was selected for an oral presentation at the 2023 Annual Myotonic Dystrophy Foundation (MDF) Conference
Larissa won first place for her poster at the 2023 CAG Triplet Repeat Disorders Gordon Research Conference
Larissa was given an award for the best talk from a postdoctoral fellow at the 2023 annual Pathology & Immunology Trainee Symposium
Matt Penna’s paper on Limch1 alternative splicing function in skeletal muscle development was published in Life Sciences Alliance
Janel Peterson was the winner of the 2023 Rolanette and Berdon Lawrence Family Achievement Award in Genetics for the Department of Molecular and Human Genetics as a PhD student in the Genetics & Genomic Program
Rong-Chi Hu was awarded a predoctoral fellowship from the American Heart Association starting Jan. 1, 2023
Janel Peterson was awarded an NIH F31 predoctoral fellowship for her proposal to study the role of smooth muscle in myotonic dystrophy gastrointestinal disturbances starting Dec. 15, 2022
Janel Peterson's extensive review titled “Clinical and molecular insights into gastrointestinal dysfunction in myotonic dystrophy types 1 & 2” was published in Int J Mol Sci 2022 Nov 26;23(23):14779
Larissa Nitschke’s paper describing the mechanism by which loss of MBNL1 results in upregulation of MBNL2 was accepted in Nucleic Acids Research
Matt Penna expertly defended his Ph.D. thesis and will return to medical school January 2023
Dr. Cooper was awarded the Steinert Award for Excellence in Myotonic Dystrophy Basic Science Research at the 13th International Myotonic Dystrophy Consortium Meeting held in Osaka, Japan
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
Credit
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.
Image of the Month: From the Labs blog
