Dr Alessia Buscaino
Senior Lecturer in Fungal Epigenetics
School of Biosciences
- 01227 (82)4854
Dr Alessia Buscaino graduated in Molecular Biology at the University of Palermo (Italy) in 2000.
She conducted her PhD research in the laboratory of Dr. Asifa Akhtar at the European Molecular Biology Laboratory (EMBL-Germany) research institute. During her PhD, her interest in epigenetics and chromatin modifications flourished while investigating mechanisms of Dosage Compensation in Drosophila melanogaster. In 2005, Dr Buscaino was awarded an EMBO long-term post-doctoral fellowship to conduct research in the laboratory of Professor Robin Allshire (WTCCB-Edinburgh). During her post-doc she investigated how heterochromatin assembles on large blocks of DNA repeats in the fission yeast Schizosaccharomyces pombe.
In 2013, she obtained a EMBO short-term Fellowship to investigate the chromatin status of Candida albicans repetitive DNA elements in Judith Berman laboratory (TAU University- Tel-Aviv, Israel).
Dr Alessia Buscaino is a Senior Lecturer in Fungal Epigenetics.
Dr Buscaino’s group aim to understand how epigenetic mechanisms control fungal pathogenicity and anti-fungal drug resistance. Within these areas the group focuses on understanding how chromatin structure regulates adaptation and genome instability in Candida albicans, the most common human fungal pathogen.
Dr Buscaino's research group belongs to the “Infection and Drug Resistance Research Group” and to the “Reproduction, evolution and genomics” research group.back to top
Also view these in the Kent Academic Repository
Genetics and Epigenetics of repetitive DNA elements in the fission yeast Schizosaccharomyces pombe and the fungal pathogen Candida albicans
A surprisingly high percentage of eukaryotic genomes is formed by sequences that are repeated multiple times. For example, repeats encompass 46% of the human genome. Other genomes contain even higher proportions of repeats (most notably plants; 65% for maize, more than 70% for pine). It has been demonstrated that DNA repeats are "unstable sequences" that can potentially induce mutations and chromosomal rearrangements, a hallmark of cancer and birth defects. Therefore, organisms have developed strategy to fight against the instability of DNA repeats. One of such strategy is the assembly of a specific type of chromatin packaging: heterochromatin.
Chromatin is the structure that allows the DNA to fit insight the cells. Chromatin is formed by histone proteins: the spool that DNA winds itself around. Histones control how tightly or loose the DNA is wrapped around them. At heterochromatin, DNA is tightly associated with histone proteins. This association creates an environment that promotes genome stability at DNA repeats.
It is therefore essential to understand how DNA repeats are packaged into heterochromatin. This is one of the questions that we aim to answer.
To this end, we study heterochromatin formation in a simple model system, the unicellular yeast Schizossacaromyces pombe. We study S. pombe because its heterochromatin is very similar to the one found in higher eukaryotes but it is much simpler. In this system, we have recently developed systems to specifically dissect the process of heterochromatin assembly. Using this system we aim to identify the DNA sequences and the proteins that allow heterochromatin to be assembled and maintained though generation at DNA repeats.
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In a second project, we study heterochromatin formation in a different fungus, the pathogen Candida albicans. C. albicans is the most important fungal pathogen of warm-blooded animals. It can live inside the human body without problem, but it can cause life-threatening diseases. Pathogenic C. albicans adapts efficiently to different environments and it can acquire resistance to anti-fungal drugs. This is because, in contrast to most organisms, C. albicans can live and thrive without the right proportion genes or with missing part of a chromosome (a phenomena called genome plasticity). It was discovered that DNA repeats play an important role into the transition that transform C. albicans into a dangerous pathogen. We are investigating whether heterochromatin is formed on DNA repeats and whether this type of chromatin is modulated when C. albicans becomes a pathogen.