PIETROFORTE SARA_photoweb.jpg

Ms. Sara Pietroforte

ESR 6

Supervisor: Dr Rita Vassena (Co supervisor Dr Filippo Zambelli)

Project: Mitochondrial-driven splicing deregulation: New mechanisms to explain the loss of competence in aged oocytes

Planned secondments: UMIL (3M) & UNESP (3M)

Email: spietroforte@eugin.es

I was born in Bari, Italy. I received a Bachelor’s Degree from the University of Bari in 2016 and a Master's Degree in Medical and Pharmaceutical Biotechnology from the University of Florence (Italy) in 2019. Throughout my years of studying, I got fascinated by human reproduction, molecular biology and the genetics of male and female infertility. Consequently, I chose to perform an internship in a research group focused on the genetics of male infertility. The aim of my masters’ thesis was to evaluate the diagnostic potential of sequencing a gene panel, based on the “azoospermia mouse model”, in men affected by idiopathic Non-Obstructive Azoospermia (NOA). In this project, I enthusiastically participated in the discovery of two new genes involved in the spermatozoa meiotic arrest. Performing this project, I well understood that a gametic alteration, even if mild, could have a great impact on the correct meiotic process and, finally, on the embryo development.

From September 2019 to February 2020, I worked as a researcher at the Fundaciò Puigvert (Barcelona, Spain) Department of Molecular Biology Laboratory as part of the Erasmus+ Traineeship programme. My project aimed at investigating novel genetic factors involved in meiotic arrest to explain spermatogenic impairments in NOA men by Next Generation Sequencing.

Studying and working in international environments allowed me to learn the preciousness of multicultural exchange and knowledge sharing, while actively contributing to science and society development. Moreover, during these years, my interest in the molecular biology of human reproduction and embryology has broadened.

The project I will be working on aims at understanding the molecular factors responsible for the decay in oocyte quality observed in women of advanced maternal age. The hypothesis that I will be testing is that mitochondrial dysfunction observed in aged tissues is responsible for a dysregulation of the splicing processes that define the transcriptome of the mature oocytes, responsible for both oocyte maturation and a correct embryonic development during the first cleavages. Unraveling the interplay between mitochondrial metabolism and alternative splicing is a novel and exciting field of research, and we will use a combination of sequencing and imaging strategies to be able to test if such deregulation happens in oocyte of women of advanced maternal age, and with the use of animal models we will investigate their function and regulation.