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!
Front Mol Neurosci 11:104
April 04, 2018
Christina's first first-author research article. We describe a patient mutation in KDM5C which has altered gene regulatory function in neurons.
May 29, 2017
Bobby's first first-author research paper published.
Cell Rep. 14(5):1000-9.
February 09, 2016
Characterization of Kdm5c-Knockout mice. These mice will be valuable for future therapeutic development of intellectual disability and autism spectrum disorders.
Nat Commun. ;6:6002. doi: 10.1038/ncomms7002.
January 22, 2015
The first paper from the lab! We developped a new RNA-seq method which allows us to profile full-length transcripts.
We found that ADD domain of ATRX, which is enriched with ATRX-syndrome mutations, is a reading module for heterochromatin histone methylation status, low H3K4me and hight H3K9me3.
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.