Non-coding genome function and diabetes
Event details
| Date | 24.04.2017 |
| Hour | 13:30 › 14:30 |
| Speaker | Jorge FERRER Imperial College, London, UK & Genomic Programming of Beta-cells Laboratory, Institut d'Investigacions August Pi I Sunyer (IDIBAPS), CIBERDEM, Barcelona, Spain |
| Location | |
| Category | Conferences - Seminars |
SEMINAR SERIES: Trends in Physiology and Metabolism (Bio-682)
Abstract:
Most genetic mechanisms that are currently known to underlie developmental processes and human diseases are based on the analysis of a very small fraction of the genome that encodes for protein-coding sequences. However, recent studies have uncovered large portions of the genome that contain functional regulatory elements and noncoding transcripts. It is thus reasonable to presume that understanding the function of such elements can shed new light into developmental and cellular mechanisms, and uncover new causes of human disease. The elucidation of noncoding defects will require knowledge of the genomic location of functional noncoding elements in disease-relevant cell types, as well as an in depth understanding of how they function. I will discuss how integrative human islet chromatin maps can provide novel insights into how the islet epigenome shapes cell-specific transcriptional programs. Existing data suggests that variation in islet lncRNAs and long-range regulatory elements contributes to the molecular mechanisms underlying human diabetes.
Abstract:
Most genetic mechanisms that are currently known to underlie developmental processes and human diseases are based on the analysis of a very small fraction of the genome that encodes for protein-coding sequences. However, recent studies have uncovered large portions of the genome that contain functional regulatory elements and noncoding transcripts. It is thus reasonable to presume that understanding the function of such elements can shed new light into developmental and cellular mechanisms, and uncover new causes of human disease. The elucidation of noncoding defects will require knowledge of the genomic location of functional noncoding elements in disease-relevant cell types, as well as an in depth understanding of how they function. I will discuss how integrative human islet chromatin maps can provide novel insights into how the islet epigenome shapes cell-specific transcriptional programs. Existing data suggests that variation in islet lncRNAs and long-range regulatory elements contributes to the molecular mechanisms underlying human diabetes.
Links
Practical information
- Informed public
- Free
Organizer
- Prof. Lluis Fajas (UNIL), Prof. Kei Sakamoto (NIHS) and Prof. Kristina Schoonjans (EPFL)
Contact
- Prof. Lluis Fajas (UNIL) - [email protected]