Russian Journal of Genetics: Applied Research. Vol. 7, No. 2, Pages 172-174, 2017

Yu. V. Andreychuk^a^,*, A. A. Shiryaeva^a^,**, A. S. Zhuk^a^,^b^,***, E. I. Stepchenkova^a^,^b^,****, and S. G. Inge-Vechtomov^a^,^b^,*****
Translated by E. Kyrova

^aInstitute of Translational Biomedicine, St. Petersburg State University, St. Petersburg, Russia

^bVavilov Institute of General Genetics, St. Petersburg Branch, Russian Academy of Sciences, St. Petersburg, Russia

Correspondence to: *e-mail: Yullinnabk@yandex.ru
Correspondence to: **e-mail: annabiologic@gmail.com
Correspondence to: ***e-mail: ania.zhuk@gmail.com
Correspondence to: **** e-mail: stepchenkova@gmail.com
Correspondence to: *****e-mail: ingevechtomov@gmail.com

Abstract—Amyloidogenesis in nerve tissues cause human diseases such as Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease, and the illness of Louis Gehrig, characterized by specific neurodegenerative symptoms. The frequency of nerve cells with an abnormal number of chromosomes is increased in patients with Alzheimer’s disease. However, the direct impact of prions on the genome stability has not been sufficiently investigated. In our work, we studied the impact of the [PSI+] prions on the stability of the S. cerevisiae genome using the alpha-test system.

Impact of Prionization of the Sup35 Protein [PSI+] on the Frequency of Genetic Changes, Accounted in the Alpha-Test in Yeast Saccharomyces cerevisiae