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Summer convective systems (CSs) initiated over the Tibetan Plateau identified by the International Satellite Cloud Climatology Project (ISCCP) deep convection database and associated Tropical Rainfall Measuring Mission (TRMM) precipitation for 1998-2001 have been analyzed for their basic characteristics in terms of initiation, distribution, trajectory, development, life cycle, convective intensity, and precipitation. Summer convective systems have a dominant center over the Hengduan Mountain and a secondary center over the Yaluzangbu River Valley. Precipitation associated with these CSs contributes more than 60% of total precipitation over the central-eastern area of the Tibetan Plateau and 30%-40% over the adjacent region to its southeast. The average CS life cycle is about 36 h; 85% of CSs disappear within 60 h of their initiation. About 50% of CSs do not move out of the Tibetan region, with the remainder split into eastwardand southward-moving components. These CSs moving out the Tibetan Plateau are generally larger, have longer life spans, and produce more rainfall than those staying inside the region. Convective system occurrences and associated rainfall present robust diurnal variations. The midafternoon maximum of CS initiation and associated rainfall over the plateau is mainly induced by solar heating linked to the unique Tibetan geography. The delayed afternoon-late night peak of rainfall from CSs propagating out of this region is a combined outcome of multiple mechanisms working together. Results suggest that interactions of summer Tibetan CSs with the orientation of the unique Tibetan geography and the surrounding atmospheric circulations are important for the development, intensification, propagation, and life span of these CSs.

Nuclear filamentous actin (F-actin) is essential for nucleocapsid morphogenesis of lepidopteran nucleopolyhedroviruses. Previously, we had demonstrated that Autographa californica multiple nucleopolyhedrovirus (AcMNPV) BV/ODV-C42 (C42) is involved in nuclear actin polymerization by recruiting P78/83, an AcMNPV orf9-encoded N-WASP homology protein that is capable of activating an actin-related-protein 2/3 (Arp2/3) complex to initiate actin polymerization, to the nucleus. To further investigate the role of C42 in virus-induced actin polymerization, the recombinant bacmid vAc p78/83nls-gfp , with a c42 knockout, p78/83 tagged with a nuclear localization signal coding sequence, and egfp as a reporter gene under the control of the Pp10 promoter, was constructed and transfected to Sf9 cells. In the nuclei of vAc p78/83nls-gfp -transfected cells, polymerized F-actin filaments were absent, whereas other actin polymerization elements (i.e., P78/83, G-actin, and Arp2/3 complex) were present. This in vivo evidence indicated that C42 actively participates in the nuclear actin polymerization process as a key element, besides its role in recruiting P78/83 to the nucleus. In order to collect in vitro evidence for the participation of C42 in actin polymerization, an anti-C42 antibody was used to neutralize the viral nucleocapsid, which is capable of initiating actin polymerization in vitro. Both the kinetics of pyrene-actin polymerization and F-actin-specific staining by phalloidin indicated that anti-C42 can significantly attenuate the efficiency of F-actin formation compared to that with control antibodies. Furthermore, we have identified the putative pocket protein binding sequence (PPBS) on C42 that is essential for C42 to exert its function in nuclear actin polymerization.