New thesis on the two SNAP-25 splicing variants; SNAP-25a and SNAP-25b
Teresa Daraio will defend her thesis "Studies of SNAP-25 in regulated membrane fusion; metabolic consequences and tuning of intracellular Ca2+ dynamics in beta cells" on October 27, 2017. Her main supervisor is Christina Bark.
What´s the main focus of your thesis?
To investigate the role of the SNAP-25 splicing variants; SNAP-25a and SNAP-25b, in metabolism with emphasis on insulin secretion and islet physiology.
Which are the most important results?
- The correct function of the SNARE complex mediating exocytosis of neurotransmitters and hormones is essential for health. Minor alteration to it, such as replacing SNAP-25b with SNAP-25a, results in metabolic syndrome in mice which is characterized by hyperinsulinemia, insulin resistance, hyperglycemia, liver steatosis and dyslipidemia.
- SNAP-25b-deficiency in islets causes increased insulin secretion associated with loss of preciseness of calcium dynamics among beta cells upon glucose stimulation.
- The SNAP-25 splicing isoforms mediate different interactions for proteins important for initiation and termination of membrane fusion events.
How can this new knowledge contribute to the improvement of people’s health?
Increased insulin secretion and insulin resistance are regarded as consequences of the metabolic syndrome. In this thesis, we have experimentally demonstrated that altered release of insulin contributes to the development of the metabolic syndrome. It is tempting to speculate that any minor modification to genes in humans is also important for exocytosis and might contribute to the progression of metabolic disease.
What are your future ambitions?
I have a particular interest in clinical research, and would like to continue working within the field of metabolism and associated diseases.