The lack of amplification in mTERC deficient cells could be related to a defect in the stabilization of the ends of the amplified chromosomes in the absence of telomerase, to a more general effect of telomerase in the regulation of gene expression, including genes involved in amplification, or to a possible interaction of the telomerase RNA with proteins involved in gene amplification.Toronto, Canada Area Professor at Sheridan College Higher Education Education University of Toronto - Ontario Institute for Studies in Education 1997 - 1999 Masters of Education ~ Human Development and Applied Psychology, Developmental and Child Psychology Ryerson University 1993 - 1996 Bachelor Applied Arts, Early Childhood Education Algonquin College of Applied Arts and Technology 1981 - 1983 Diploma ~ Early Childhood Education, Early Childhood Education Experience Community College ProfessorSheridanApril 1999 - Present Eagles Nest Project - Consultant 1996 - 1997 Saskatchewan Institute Applied 1995 - 1997 Hanen Language Centre 1994 - 1995 The Learning Enrichment Foundation 1988 - 1993 St-Lawrence College 1987 - 1988 Non-Profit Child Care Centres 1982 - 1988 Skills Child Development, Workshop Facilitation, Leadership, Early Childhood., Teaching, Mental Health, Curriculum Development, Leadership developement, Theory, Research, Academic Advising, Career Counseling, Social Services, Volunteer, Nonprofits, First Nations, Infant and Toddler, Child Care, Attachment Theory, Attachment Parenting, Educational Technology, Child and family., E-Learning, Training, family support Show more The causal relationship between mTERC deficiency and lack of gene amplification was demonstrated by the restoration of CAD gene amplification in two of the three deficient cell lines transfected with mTERC. As expected, in 9 out of 10 N-(phosphonacetyl)-l-aspartate (PALA) resistant clones derived from wild-type cells, CAD was amplified in contrast, in none of the 30 PALA resistant clones isolated from the three mTERC−/− cell lines we could detect CAD amplification, indicating that, in the absence of telomerase activity, gene amplification is inhibited. To investigate whether telomerase, the enzyme deputed to telomere maintenance, also plays a role in gene amplification, we studied the amplification of the carbamyl-P-synthetase, aspartate transcarbamilase, dihydro-orotase (CAD) gene in immortalized embryonic fibroblasts derived from telomerase knockout mice (mTERC−/−) of the first and of the sixth generation. Mutations in genes important for the preservation of genome stability can increase the frequency of gene amplification, a process relevant to tumor development. Rebuzzini, Paola Martinelli, Paola Blasco, Maria Giulotto, Elena Mondello, Chiara
Inhibition of gene amplification in telomerase deficient immortalized mouse embryonic fibroblasts Inhibition of gene amplification in telomerase deficient immortalized mouse embryonic fibroblasts
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