The main aim of the lab of lab is to work on beta-cell regulatory genomics, genetics, and modeling diabetes to find new therapies.
Professor Ferrer is interested in understanding the genome regulation of pancreatic beta cells and its implications for human diabetes. His team has combined genetic model systems and advanced genomics to address key questions in human beta cell biology, regeneration, and disease.
Diabetes mellitus afflicts more than 400 million people. Current strategies to prevent and treat diabetes are limited by our scant knowledge of the molecular defects that cause diabetes. We focus on understanding changes in genome regulation that lead to monogenic and polygenic diabetes. We study the gene networks that are essential for insulin-producing beta cells to maintain glucose homeostasis, and develop strategies to manipulate these networks in human patients. We are also interested in how gene regulatory mechanisms can be harnessed for regenerative therapies in autoimmune diabetes. To achieve these goals, we combine regulatory genomics, human genetics, and genome engineering in model systems.
Merits of the lab:
The lab created the first genome maps of human pancreatic regulatory elements, and defined the role of noncoding variants in polygenic type 2 diabetes, and in rare Mendelian forms of diabetes. It coordinates a project to discover genetic mechanisms of diabetes through whole genome sequencing of a large cohort of patients with non-autoimmune young-onset diabetes. It combines mouse genetics, genome editing, single cell genomics and stem cell differentiation models to understand the role of noncoding defects in human disease.
Why do we want medical doctors?
The team is highly multidisciplinary. It is composed of members with diverse backgrounds (biotechnology, biology, medical, engineering) and includes individuals with expertise in computational genomics, human genetics, single cell genomics, mouse genetics and genome editing in human stem cells.
Our lab is focused on the study of the genetic mechanisms of diabetes by the use of high-throughput genomics sequencing.
How we will do it?
We offer two alternative projects:
One is to use computational approaches to discover new mechanisms of diabetes in whole-genome sequences from a large cohort of patients with early-onset non-autoimmune diabetes. The successful candidate will lead a specific project, working together with a multidisciplinary team of computational, clinical, and experimental scientists.
An alternative project that is offered is to lead a project that uses genome editing approaches and stem cell differentiation models to understand the underlying mechanisms of noncoding genome defects that cause human diabetes.
Why is this important?
Sequencing of whole patient genomes is rapidly acquiring a central role in modern medicine. Existing strategies have been very successful in identifying disease-causing variants in protein-coding portions of the genome. By contrast, the interpretation of genetic variants in the remaining >98% of the genome, remains largely unsolved. The CRG group has been instrumental in deciphering the role of noncoding variants in polygenic diabetes and rare monogenic diabetes. It has now created patient genome cohorts and experimental models to tackle this problem systematically. These efforts promise to discover new genetic mechanisms, uncover new insights into biological processes that have been disrupted by natural mutations, and understand the mechanisms of disease.
Who is a good fit for the project?
Candidates for the human genetics position should have some previous expertise in programming or statistical analysis.
Candidates for the stem cell modeling project should have experience in cell culture and molecular biology.
IDIBAPS#1 – Developing and investigating computing, machine learning and physiological modelling for understanding each individual heart towards personalised medicineDavid Brena2022-05-17T10:37:53+00:00