Molly Hammell (Milton E. Cassel Scholar) holds a B.S. in physics from the College of William and Mary and a Ph.D. in physics and astronomy from Dartmouth College. The Hammell lab specializes in developing novel computational algorithms for the analysis and integration of high-throughput genomics datasets and applying these to questions of human disease. Hammell has a broad background in small RNA biology and gene regulatory network analysis, transposon biology and genomics, as well as extensive experience in the statistical analysis of next-generation sequencing data. As a postdoctoral fellow working with Victor Ambros at Dartmouth Medical School and the University of Massachusetts Medical School, she developed new algorithms to identify the targets and pathways regulated by microRNAs in animals and to profile the dynamics of small RNA activity across development. Her lab at Cold Spring Harbor Laboratory has expanded on these efforts to map the role of both microRNAs and transposon-targeting piRNAs and siRNAs in animals. This includes efforts to establish the molecular mechanisms by which transposons are controlled in somatic tissues. This also includes a major project to profile the genomes and transcriptomes of amyotrophic lateral sclerosis (ALS) patient samples in order to understand the extent to which transposons contribute to neurodegenerative disease in patients.
Our genomes are filled with viral-like sequences called transposons, many of which are capable of creating new copies of themselves that can reintegrate elsewhere in the genome, altering the function of nearby genes. While most transposon sequences are now-defunct remnants of ancient genomic parasites, a small fraction of these are still capable of activating themselves, creating genomic instability and crippling cellular function. The Hammell lab and others have discovered a link between the activity of these transposon sequences and neurodegenerative diseases related to misfunction of the RNA binding protein TDP-43 (ALS and frontotemporal lobar degeneration). However, much remains unknown about how transposons are controlled in somatic tissues such as the brain, and the extent to which their activity contributes to neurodegenerative disease. Hammell’s group is working to elucidate the connections between transposon activity and TDP-43 related diseases.