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met1 DNA Methyltransferase Controls TERT Gene Expression: A New Insight to The Role of Telomerase in Development
OBJECTIVE: DNA methylation systems are essential for proper embryo development. Methylation defects lead to developmental abnormalities. Furthermore, changes in telomerase gene expression can affect stability of chromosomes and produces abnormal growth. Therefore, defects in both methylation and tel...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Royan Institute
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6791074/ https://www.ncbi.nlm.nih.gov/pubmed/31606969 http://dx.doi.org/10.22074/cellj.2020.6290 |
Sumario: | OBJECTIVE: DNA methylation systems are essential for proper embryo development. Methylation defects lead to developmental abnormalities. Furthermore, changes in telomerase gene expression can affect stability of chromosomes and produces abnormal growth. Therefore, defects in both methylation and telomerase gene expression can lead to developmental abnormalities. We hypothesized that mutation in the methylation systems may induce developmental abnormalities through changing telomerase gene expression. MATERIALS AND METHODS: In this experimental study, we used Arabidopsis thaliana (At) as a developmental model. DNA was extracted from seedlings leaves. The grown plants were screened using polymerase chain reaction (PCR) reactions. Total RNA was isolated from the mature leaves, stems and flowers of wild type and met1 mutants. For gene expression analysis, cDNA was synthesized and then quantitative reverse transcription PCR (qRT-PCR) was performed. RESULTS: Telomerase gene expression level in homozygous met1 mutant plants showed ~14 fold increase compared to normal plants. Furthermore, TERT expression in met1 heterozygous was~ 2 fold higher than the wild type plants. CONCLUSION: Our results suggested that TERT is a methyltransferase-regulated gene which may be involved in developmental abnormities causing by mutation in met1 methyltransferase system. |
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