Yeast RAD2, a homolog of human XPG, plays a key role in the regulation of the cell cycle and actin dynamics
| Autor: | Sung Haeng Lee, Sung-Lim Yu, Mi-Sun Kang, Sung-Keun Lee, Ho-Yeol Kim, Byung Hyune Choi, Choco Michael Gorospe |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2013 |
| Předmět: |
Genetics
Xeroderma pigmentosum biology QH301-705.5 Cell growth DNA damage Science Saccharomyces cerevisiae Cell cycle medicine.disease biology.organism_classification General Biochemistry Genetics and Molecular Biology Cockayne syndrome Cell biology Transcription (biology) Cell polarity medicine Biology (General) Actin dynamics General Agricultural and Biological Sciences RAD2 Research Article |
| Zdroj: | Biology Open Biology Open, Vol 3, Iss 1, Pp 29-41 (2013) |
| ISSN: | 2046-6390 |
| Popis: | Summary Mutations in the human XPG gene cause Cockayne syndrome (CS) and xeroderma pigmentosum (XP). Transcription defects have been suggested as the fundamental cause of CS; however, defining CS as a transcription syndrome is inconclusive. In particular, the function of XPG in transcription has not been clearly demonstrated. Here, we provide evidence for the involvement of RAD2, the Saccharomyces cerevisiae counterpart of XPG, in cell cycle regulation and efficient actin assembly following ultraviolet irradiation. RAD2 C-terminal deletion, which resembles the XPG mutation found in XPG/CS cells, caused cell growth arrest, the cell cycle stalling, a defective α-factor response, shortened lifespan, cell polarity defect, and misregulated actin-dynamics after DNA damage. Overexpression of the C-terminal 65 amino acids of Rad2p was sufficient to induce hyper-cell polarization. In addition, RAD2 genetically interacts with TPM1 during cell polarization. These results provide insights into the role of RAD2 in post-UV irradiation cell cycle regulation and actin assembly, which may be an underlying cause of XPG/CS. |
| Databáze: | OpenAIRE |
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