Please use this identifier to cite or link to this item:
https://hdl.handle.net/11147/3811
Title: | Molecular mechanisms of boron toxicity and identification of boron metabolim genes | Authors: | Uluışık, İrem | Advisors: | Koç, Ahmet | Publisher: | Izmir Institute of Technology | Abstract: | Boron is an essential micronutrient for plants and it is either necessary or beneficial for animals. Studies identified only few genes related to boron metabolism thus far and details of how boron is imported into cells and used in cell metabolism are largely unknown. In this study, in order to identify genes that play role in boron metabolism, the entire set of yeast haploid deletion mutants was screened and 6 boron resistant and 21 boron sensitive mutants were identified. Boron treatment activated the expression of ATR1 and many genes that are regulated by genereal amino acid control in a GCN4 dependent manner. Polysome analyses and 35-S methionine labelling assays suggested that boron inhibits protein synthesis. Inhibition of protein synthesis was also confirmed by the phosphorylation of translation factor eIF2. in boron treated cells, and phosphorylation of eIF2. was totally dependent on the uncharged tRNA binding domain of Gcn2 kinase. Overall, our results revealed many genes and pathways related to boron stress response and suggest a possible link between boron toxicity and translational control. | Description: | Thesis (Master)--Izmir Institute of Technology, Molecular Biology and Genetics, Izmir, 2010 Includes bibliographical references (leaves: 36-41) Text in English; Abstract: Turkish and English ix, 41 leaves |
URI: | http://hdl.handle.net/11147/3811 |
Appears in Collections: | Master Degree / Yüksek Lisans Tezleri |
Files in This Item:
File | Description | Size | Format | |
---|---|---|---|---|
T000829.pdf | MasterThesis | 2.23 MB | Adobe PDF | ![]() View/Open |
CORE Recommender
Page view(s)
88
checked on Aug 12, 2024
Download(s)
66
checked on Aug 12, 2024
Google ScholarTM
Check
Items in GCRIS Repository are protected by copyright, with all rights reserved, unless otherwise indicated.