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CaralinaMarin De Evsikova

Caralina Marin De Evsikova, PhD

Assistant Professor, COLLEGE OF MEDICINE MOLECULAR MEDICINE
  • The early developmental environment plays a pivotal role in susceptibility to adulthood metabolic disease, such as obesity and diabetes. The long-term goal of this project is to understand how the maternal and embryonic environment alters gene expression, which ultimately leads to disease, via epigenetics. Epigenome of each individual is established during the egg-to-embryo transition, which is sensitive to teratogens, such as alcohol, bisphenol A, or dietary exposures. To identify the role of epigenetics in metabolic disease, I am using a naturally occurring “epigenetic barometer” allele (viable yellow) of the Agouti gene in mice, whose expression is controlled by methylation levels. Nutrigenomics & Healthspan. My long-term goal is to develop new mouse models of adult-onset metabolic diseases by monitoring in vivo physiology coupled with quantitative molecular genetics to detect genes and pathways involved with weight gain. This approach has been successful in identifying changes in eating, activity, and loss of circadian rhythms underlying “normal” weight fluctuations from across the lifespan.
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Post Docs

  • The Ferreira laboratory focuses on the heme biosynthetic pathway, which consists of eight enzyme-catalyzed reactions. Heme biosynthesis occurs under the control of the enzyme 5-Aminolevulinate synthase (ALAS), which catalyzes the first and rate-limiting reaction of succinyl-CoA with glycine to produce 5-aminolevulinate (ALA), CoA, and CO2. Loss-of-function and gain-of-function mutations in human erythroid ALAS (ALAS2) have been associated with two diseases, x-linked sideroblastic anemia (XLSA) and x-linked dominant protoporphyria (XLDPP), respectively. In XLDPP, the gain-of-function of the ALAS2 enzyme causes extreme photosensitivity resulting from protoporphyrin IX accumulation in the skin of patients. Although the mutations associated with XLSA occur throughout the ALAS2 gene, those associated with XLDPP all correspond to modifications in the C-terminus of the mature enzyme. The 26 C-terminal amino acids of mature ALAS2 are highly conserved, and yet differ from those in ALAS1, the housekeeping ALAS isoform, suggesting that the C-terminus may play an important role in erythroid-specific regulation. The overall hypothesis of my project is that the C-terminal region of ALAS2 provides specific regulatory mechanisms of heme biosynthesis to precursor erythroid cells.
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Ph.D. Students

SarahFontaine

Sarah Fontaine, PhD

Postdoctoral Scholar Research, COLLEGE OF MEDICINE MOLECULAR MEDICINE
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