INFLUENCE OF WEATHER FACTORS ON INCIDENCE OF SHOOT AND FRUIT BORER (Earias vittella Fabiricus) ON BHENDI

The field experiments were carried out in the farmer field at C. Mutlur near Chidambaram during rabi and kharif 2017. The results of experiments revealed that the per cent shoot damage and fruit damage by E. vittella on bhendi  reached peak on 13th and 15th MSW in rabi season, whereas 43rd and 42nd MSW in kharif season. The per cent shoot damage and fruit damage by E. vittella were exerted significantly positively correlated with minimum (0.552 & 0.698) and maximum temperature (0.629 & 0.748), whereas rainfall positively correlated with per cent shoot and fruit damage but it was non significant (0.111 & 0.297), however relative humidity (-0.178 & -0.210) and sunshine hours were exerted negatively correlated with per cent shoot damage and fruit damage by E. vittella during rabi 2017. The kharif season 2017 indicated that per cent shoot damage and fruit damage of bhendi was positively non significant association with RH and rain fall, while negatively non significant correlation with minimum temperature (-0.43 & -0.309) and sunshine hours (-0.265 & -0.283) was recorded

IKKβ Regulates the Repair of DNA Double-Strand Breaks Induced by Ionizing Radiation in MCF-7 Breast Cancer Cells

Activation of the IKK-NFκB pathway increases the resistance of cancer cells to ionizing radiation (IR). This effect has been largely attributed to the induction of anti-apoptotic proteins by NFκB. Since efficient repair of DNA double strand breaks (DSBs) is required for the clonogenic survival of irradiated cells, we investigated if activation of the IKK-NFκB pathway also regulates DSB repair to promote cell survival after IR. We found that inhibition of the IKK-NFκB pathway with a specific IKKβ inhibitor significantly reduced the repair of IR-induced DSBs in MCF-7 cells. The repair of DSBs was also significantly inhibited by silencing IKKβ expression with IKKβ shRNA. However, down-regulation of IKKα expression with IKKα shRNA had no significant effect on the repair of IR-induced DSBs. Similar findings were also observed in IKKα and/or IKKβ knockout mouse embryonic fibroblasts (MEFs). More importantly, inhibition of IKKβ with an inhibitor or down-regulation of IKKβ with IKKβ shRNA sensitized MCF-7 cells to IR-induced clonogenic cell death. DSB repair function and resistance to IR were completely restored by IKKβ reconstitution in IKKβ-knockdown MCF-7 cells. These findings demonstrate that IKKβ can regulate the repair of DSBs, a previously undescribed and important IKKβ kinase function; and inhibition of DSB repair may contribute to cance cell radiosensitization induced by IKKβ inhibition. As such, specific inhibition of IKKβ may represents a more effective approach to sensitize cancer cells to radiotherapy