Based on the data analysis of the 1000 hPa wind, SST and SSH anomalies, it is revealed that the atmospheric variations associated with Indian Ocean Dipole (IOD, or referred as Indian Ocean Zonal Dipole Mode, IOZDM) consist of a pair of anticyclones closely north and south of the equator with accompanying intense equatorial easterly anomalies, while the atmospheric variations related to El Niño/Southern Oscillation (ENSO) include a strong anticyclone in the southeastern tropical Indian Ocean (TIO) at higher latitudes with strong along‐shore wind anomalies near Java‐Sumatra coast. The different atmospheric forcing patterns lead to the fact that oceanic thermocline variations associated with IOD/IOZDM are more closely confined to the region north of 10°S, while ENSO‐induced thermocline variations are dominant south of 10°S.

The response of the Indian Ocean dipole (IOD) mode to global warming is investigated based on simulations from phase 5 of the Coupled Model Intercomparison Project (CMIP5). In response to increased greenhouse gases, an IOD-like warming pattern appears in the equatorial Indian Ocean, with reduced (enhanced) warming in the east (west), an easterly wind trend, and thermocline shoaling in the east. Despite a shoaling thermocline and strengthened thermocline feedback in the eastern equatorial Indian Ocean, the interannual variance of the IOD mode remains largely unchanged in sea surface temperature (SST) as atmospheric feedback and zonal wind variance weaken under global warming. The negative skewness in eastern Indian Ocean SST is reduced as a result of the shoaling thermocline. The change in interannual IOD variance exhibits some variability among models, and this intermodel variability is correlated with the change in thermocline feedback. The results herein illustrate that mean state changes modulate interannual modes, and suggest that recent changes in the IOD mode are likely due to natural variations.

Late generations of telomerase-null (TR(-/-)) mice exhibit progressive defects in highly proliferative tissues and organs and decreased fertility, ultimately leading to sterility. To determine effects of telomerase deficiency on germ cells, we investigated the cleavage and preimplantation development of embryos derived from both in vivo and in vitro fertilization of TR(-/-) or wild-type (TR(+/+)) sperm with either TR(-/-) or TR(+/+) oocytes. Consistently, fertilization of TR(-/-) oocytes with either TR(+/+) or TR(-/-) sperm, and TR(-/-) sperm with TR(+/+) oocytes, resulted in aberrant cleavage and development, in contrast to the normal cleavage and development of TR(+/+) oocytes fertilized by TR(+/+) sperm. Many (>50%) of the fertilized TR(-/-) eggs developed only one pronucleus, coincident with increased incidence of cytofragmentation, in contrast to the normal formation of two pronuclei and equal cleavage of wild-type embryos. These results suggest that both TR(-/-) sperm and oocytes contribute to defective fertilization and cleavage. We further found that a subset (7-9%) of telomeres was undetectable at the ends of some metaphase I chromosomes from TR(-/-) spermatocytes and oocytes, indicating that meiotic germ cells lacking telomerase ultimately resulted in telomere shortening and loss. Dysfunction of meiotic telomeres may contribute to aberrant fertilization of gametes and lead to abnormal cleavage of embryos, implying an important role of functional telomeres for germ cells undergoing fertilization and early cleavage development.