To conduct a study of understanding the molecular mechanism of genomic imprinting and developing the novel molecular therapy for genomic imprinting disorders of Prader-Willi and Angelman syndrome using small molecule and CRISPR/Cas9 genome editing approach (see our recent paper PMID:28024084 for the detail).
To conduct a study of understanding how epigenetics contributes to the brain function and how epigenetic dysregulations in the DNA methylation and histone modification are implicated in neurodevelopmental disorders. We will use mutant mice in genes that are strongly supported by the human genetics discovery from patients with autism and neurodevelopmental disorders. We will use the epigenetics and molecular neurobiology techniques to study
To conduct a study of understanding the molecular and circuitry mechanisms underlying SHANK2 and SHANK3 causing autism and neuropsychiatric disorders using genetically modified mouse models, and developing target specific treatments (PMID: 27161151, 23583105, 29046483, 29097328). We will use the molecular, behavioral, and in vivo circuitry analyses including chemogenetics and optogenetics tools in mouse models.
Neurobiology and Genetics programs at Duke University School of Medicine offer exciting research environment for trainees
The candidate should have a PhD or MD/PhD in neuroscience, genetics, and molecular biology . Experience in molecular neurobiology, mouse behavioral analysis, in vivo recording, and optogenetics is preferred.
Additional Salary Information: Based on the years of experience
Internal Number: 40042018
About Duke University School of Medicine
The research in Jiang’s lab is directed at understanding genetic and epigenetic basis of human diseases with a focus on genomic imprinting disorders of Angelman and Prader-Willi syndrome as well as autism spectrum disorders. Angelman syndrome and Prader-Willi syndrome are two best examples of genomic imprinting disorders caused by the defect of an imprinting domain in the human chromosome 15q11-q13 region. Autism spectrum disorders are neurodevelopmental disorder that affects 1 out 160 children. The core symptoms of autism spectrum disorders are impairment in communication and language development, social interaction, and stereotyped behaviors. Although the strong genetic etiology is implicated in autism spectrum disorders, the molecular basis for majority of individuals with autism spectrum disorders remains unknown. From lessons learned from genomic imprinting disorder of Angelman syndrome, we hypothesize that both genetic and epigenetic defects in genes encoding synaptic proteins contribute to the susceptibility of autism spectrum disorders.
We are using genetic and epigenetic tools to identify the molecular basis of autism spectrum disorders. For genetic analysis, we are ai...ming to identify DNA mutation and chromosomal microdeletion of synaptic protein coding genes in autism spectrum disorders. For epigenetic analysis, we are particularly interested in the role of DNA methylation in the susceptibility of autism spectrum disorders and brain function. Using mouse embryonic stem cell gene targeting and other mouse genetic manipulations, we have generated a panel of mutant mice to study human Angelman and Prader-Willi syndrome as well as autism spectrum disorders. Using techniques combining biochemical, morphological, electrophysiological, and behavioral analysis, we are dissecting the function of human disease causing genes in vivo, understanding the function of DNA methylation in brain function, and delineating the synaptic basis of neurodevelopmental disorders in mouse models.