Chrissa Kioussi grew up in Athens, at the foothills of Akropolis during the school year and on the Aegean islands during the summer. She graduated from the University of Athens with a major in Biology and a Diploma in Biochemistry. She earned her PhD in Cell and Molecular Biology from the Hellenic Pasteur Institute. She discovered her love for developmental biology and mouse molecular genetics during her postdoctoral years at the Max-Plack Institute of Biophysical Chemistry in Germany. She landed at the coast of Southern California, at HHMI-UCSD, to research the transcriptional regulation of homeobox genes during organ formation. She brought this expertise to the Pacific Northwest, where she established her lab at Oregon State University.
Organ Development and Tissue Regeneration
The goal of regenerative medicine is to build body parts to correct birth defects in newborns or replace body parts in the aging. Mammalian cells that are reset to the proper developmental state appear to have the ability to integrate into aged or improperly formed tissues and organs. Such reprogrammed cells can form replacement body parts, and thus it is necessary to understand the mechanisms that genomes use to create the many cell, tissue, and organ types. Cell types are defined at the molecular level during embryogenesis by a process called pattern formation. The Kioussi lab is interested in studying the developmental programs that define the gene network available to each particular cell type in the body, and the molecular interactions used at any given time and place.
Myogenesis
Congenital myopathies and muscular dystrophies cause reduction of muscle size and/or tone, muscle weakness and locomotive disabilities. During embryogenesis, sequential phases of myogenesis lead to the formation of the skeletal musculature. We study the gene networks involved in developmental and disease states of the skeletal muscle system.
Cardiogenesis
Congenital heart defects in humans occur in approximately 1% of live births and are a leading cause of miscarriages. One of the most important reasons for this high mutagenic incidence is that the heart is the first organ to form and must be active at all stages as it develops its remarkably complex structure. We study the mechanisms of many human congenital cardiac syndromes and defects at the cellular and molecular level, with the ultimate goal to develop treatments and cures.
Cell Reprogramming
Adult somatic cells are tightly fixed into stable cellular states by epigenetic mechanisms that consolidate the transcriptional network states achieved during embryogenesis. The sustained artificial expression of specific combinations of transcription factors can reprogram cells to a different developmental state. We can convert adult biopsy cell cultures into specific neurons, muscles or cardiomyocytes.
