The University of Michigan Medical School
Human Genetics Department
Ann Arbor, MI, 48108
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FEBS J. 2022 Apr;289(8):2301-2317.
We examine how impaired germline gene repression by chromatin regulators may lead to impaired brain development & function in certain neurodevelopmental disorders (NDDs). We also discuss how to test hypotheses to determine the contribution of ectopic germline transcripts to chromatin-NDDs.
Genome Res. 2021 Jan 7;31(2):186-197.
We found that loss of Kdm1a in mouse neurons lead to premature activation of neuronal activity-dependent enhancers & genes. A basic research step towards understanding the associated human KDM1A / LSD1 neurodevelopmental syndrome.
Cell Rep. 2020 Aug 11;32(6):108002.
August 10, 2020
We devised metabolic labeling of nascent RNAs and sequencing in the neural ensemble. Using this approach, we found a role of RAI1, Smith-Magenis Syndrome gene, in neuronal-activity dependent transcription and synaptic plasticity. Great collaboration with Dr. Michael Sutton lab at Michigan Neuroscience Institute.
Communications Biology 2020 Jun 1;3(1):278.
June 01, 2020
We found mutually suppressive roles of H3K4me writer KMT2A and eraser KDM5C. This work provides proof of the principle of modulating single methyl histone enzymes to ameliorate neurodevelopmental disorders. Great collaboration with Tronson Lab!
Cell. 128(6):1077-88. Epub 2007 Feb 22.
February 22, 2007
We discovered the first family of enzymes which can remove H3K4me3. One of the family members, JARID1C/KDM5C was known to be mutated in X-linked intellectual disability. We linked hitone methylation dynamics and human cognitive development for the first time.