Upon DNA damage, plants and animals halt cell division and execute DNA repair. This response prevents the damaged cells from proliferating. NAIST Professor Masaaki Umeda has made a career studying the molecular biology behind this protective measure.
"We reported that SOG1 is activated by DNA damage and regulates almost all genes induced by the damage," he says. Another study from the lab showed "Rep-MYBs are stabilized in DNA damage conditions to suppress cell division," he adds.
Laboratory - Study - Umeda - Research - Team
In the laboratory's newest study, Umeda's research team shows that ANAC044 and ANAC085 act as a bridge between SOG1 and Rep-MYB.
The scientists disrupted DNA in Arabidopsis cells by treating the cells with bleomycin, a compound commonly used to halt the growth of human cancer cells. The Arabidopsis cells failed to proliferate as expected unless they possessed a mutation in ANAC044 or ANAC085. In the mutant cases, the cells proliferated as though they were never exposed to bleomycin.
ANAC044 - ANAC085 - Root - Growth - Retardation
"We found that ANAC044 and ANAC085 are essential for root growth retardation and stem cell death, but not for DNA repair," says Umeda.
Specifically, ANAC044 and ANAC085 were responsible for preventing the cell cycle from proceeding from G2 phase to mitosis in response to the DNA damage.
Rep-MYBs - Cause - Arrest - Cell - Cycle
Rep-MYBs cause the same arrest in the cell cycle....
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