Epigenetic changes of Arabidopsis MET1 cytosine methyltransferase mutants under salt stress

Yeşildirek Y. V., Arıkan B., Turgut Kara N.

Plant Biosystems, cilt.157, sa.3, ss.507-515, 2023 (SCI-Expanded) identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 157 Sayı: 3
  • Basım Tarihi: 2023
  • Doi Numarası: 10.1080/11263504.2023.2165567
  • Dergi Adı: Plant Biosystems
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, Agricultural & Environmental Science Database, BIOSIS, CAB Abstracts, Environment Index, Veterinary Science Database
  • Sayfa Sayıları: ss.507-515
  • Anahtar Kelimeler: abiotic stress, Arabidopsis thaliana, epigenetics, methylation, qPCR, salinity stress, telomerase
  • İstanbul Üniversitesi Adresli: Evet

Özet

© 2023 Societá Botanica Italiana.In this study, we investigated the morphological and molecular responses of Arabidopsis met1-7 and met1-3 mutants under salinity stress. Global DNA methylation changes of mutants were compared and genes known to be involved in DNA methylation in plants were analyzed. Also, the expression of the telomerase reverse transcriptase (TERT) gene as a stress response indicator was analyzed in order to examine the effects of stress on the telomerase enzyme in the mutants. We found that mutants have a higher rate of hypomethylation than Col-0, under all conditions. According to the qPCR analysis, expression levels of Domains Rearranged Methylase 2 (DRM2), Polymerase IV (Pol IV) and Polymerase V (Pol V) genes were higher in mutants than Col-0 plants. Contrary to expectations for the TERT gene, there was an increase in expression in the stress-applied mutant plants. Taken together, results suggest that the RNA-directed DNA methylation (RdDM) pathway is enhanced in mutants in order to deal with the lack of DNA methylation in CG sites. In conclusion, we believe that the morphological and molecular data obtained regarding the effects of NaCl application to met1 mutants will help us to understand the epigenetic basis of stress mechanisms.