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To guard genome integrity, response mechanisms coordinately execute the G2/M checkpoint in responding to stress. p38 MAPK is activated to prolong the G2 phase for completion of damage repair. Tlk activity is required for DNA repair, chromosome segregation and G2 recovery. However, the involvement of Tlk in G2 recovery differs from previous findings that  Tlk  overexpression delays the G2/M transition. To clarify this difference, genetic interaction experiments were performed using the second mitotic wave as model system. The results indicate that  Tlk  overexpression prolongs the G2 phase through  p38 MAPK  activation, independent of Tlk kinase activity. The results of co-immunoprecipitation, database search and RNAi screening suggest that  eEF  1  α  1  and  Hsc70-5  links  Tlk  to  Tak  1 . Reduced gene activities of  Tlk ,  Hsc70-5 ,  eEF  1  α  1  and/or  Tak  1  couldn’t prolong the G2 phase induced by heat shock, indicating that these proteins work together to elevate  p38 MAPK  activity. In contrast, a high level of wild type Tlk decreases phosphorylated p38 MAPK levels. Thus, the difference is explained by a dual function of  Tlk . When under stress, inactive Tlk increases p38 MAPK activity to prolong the G2 phase, and then activated Tlk modulates activities of p38 MAPK and Asf1 to promote G2 recovery afterwards.

Inactive Tlk associating with Tak1 increases p38 MAPK activity to prolong the G2 phase