Differential aboveground-belowground adaptive strategies to alleviate N addition-induced P deficiency in two alpine coniferous forests.

Increasing atmospheric nitrogen (N) deposition has resulted in phosphorus (P) limitation in multiple terrestrial ecosystems, yet how plants coordinate aboveground and belowground strategies to adapt to such P deficiency remains unclear. In this study, we conducted a field N fertilization experiment in two alpine coniferous plantations (Picea asperata Mast. and Pinus armandii Franch.) with different soil N availability on the eastern Tibetan Plateau of China, to examine N addition effects on plant nutrient limiting status and plant adaptive strategies corresponding to aboveground P conservation and belowground P acquisition. The results showed that N addition aggravated P deficiency in both plantations, as indicated by decreased needle P concentrations and increased N:P ratios, and that plant strategies for addressing such P deficiency differed in the two plantations with different initial soil N availabilities. In the P. asperata plantation with relatively high N availability, significantly enhanced needle phosphatase activity and shifts in P fraction allocation (downregulation of the structural P fraction and increased allocation to the residual P fraction) co-occurred with increased rhizosphere effects on phosphatase activity under N addition, indicating a synergistic strategy of aboveground P conservation and belowground P mining to alleviate P deficiency. In the P. armandii plantation with relatively low N availability, however, N addition only enhanced phosphatase activity and increased allocation to residual P fraction in the aboveground but had little effect on belowground P acquisition-associated traits, suggesting a decoupling relationship between aboveground P conservation and belowground P acquisition. This study highlights the vital significance of initial soil nutrient availability in regulating the coordination of aboveground and belowground strategic alternatives, emphasizing the need to integrate soil nutrient conditions for a holistic understanding of forest adaptation to anthropogenic N enrichment.

The expression of APE1 in triple-negative breast cancer and its effect on drug sensitivity of olaparib.

Triple-negative breast cancer is a kind of breast cancer with poor prognosis and special biological behavior, which lacked endocrine therapy and targeted therapy. We investigate the effect of human APE1 (apurinic/apyrimidyl endonuclease 1), a rate-limiting enzyme of base excision repair, on the prognosis in triple-negative breast cancer and drug sensitivity of olaparib. The expression of APE1 was detected by immunohistochemistry in the triple-negative breast cancer tissues and its effect on survival of triple-negative breast cancer patients was followed. To find whether APE1 effect the drug sensitivity in triple-negative breast cancer cells, the APE1-knockout HCC1937 cell line (triple-negative breast cancer cell line) was established by CRISPR/Cas9 system. Then, we use the wild-type and knockout one to test the drug sensitivity of olaparib. The expression of APE1 in triple-negative breast cancer tissues was significantly higher than that in the adjacent tissues (85.6% vs 14.4%) and its expression was related to tumor size (p < 0.05). We also found that it is an independent prognostic factor in patients with triple-negative breast cancer (overall survival, p = 0.01). In vitro assay, the half maximal inhibitory concentration of olaparib in HCC1937-APE1-KO was significantly increased (17.22 vs 91.85 µM) compared to the wild type. The growth curve showed that olaparib had a stronger lethality on HCC1937 compared to HCC1937- APE1-KO (p < 0.05 on day 3). HCC1937 resulted in more mitotic G2/M arrest and increased apoptosis rate after treatment with 40 µM of olaparib, while HCC1937-APE1-KO did not change significantly. When HCC1937 was treated with different concentrations of olaparib, it was found that APE1 expression decreased more significantly at 15 µM of olaparib was. In HCC1937-APE1-KO, the expression of endogenous poly (ADP-ribose) polymerase 1 was also less than that of HCC1937. These results suggested that the expression of APE1 was an important basis for the maintenance of poly (ADP-ribose) polymerase 1, and the deletion of APE1 may be related to the resistance of olaparib.