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Abstract. Budding in the yeast Saccharomyces cerevisiae involves a polarized deposition of new cell surface material that is associated with a highly asymmetric disposition of the actin cytoskeleton. Mutants defective in gene CDC24, which are unable to bud or establish cell polarity, have been of great interest with regard to both the mechanisms of cellular morphogenesis and the mechanisms that coordinate cell-cycle events. To gain further insights into these problems, we sought additional mutants with defects in budding. We report here that temperature-sensitive mutants defective in genes CDC42 and CDC43, like cdc24 mutants, fail to bud but continue growth at restrictive temperature, and thus arrest as large unbudded cells. Nearly all of the arrested cells appear to begin nuclear cycles (as judged by the occurrence of DNA replication and the formation and elongation of mitotic spindies), and many go on to complete nuclear division, supporting the hypothesis that the events associated with budding and those of the nuclear cycle represent two independent pathways within the cell cycle. The arrested mutant cells display delocalized cell-surface deposition associated with a loss of asymmetry of the actin cytoskeleton. CDC42 maps distal to the rDNA on chromosome XII and CDC43 maps near lys5 on chromosome VII.A important class of questions about the cell division cycle concerns the dependency relationships or other coordinating mechanisms that ensure that cell-cycle events occur in an appropriate sequence. Such questions have been investigated in the yeast Saccharomyces cerevisiae by using mutations and inhibitors that block specific cellcycle events (Hartwell et al., 1974;Pringle, 1978;Pringle and Hartwell, 1981; Moir and Botstein, 1982;Wood and Hartwell, 1982;Jacobs et al., 1988; Hartwell and Weinert, 1989). In this context, temperature-sensitive (Ts-) ~ mutants defective in gene CDC24 have been of great interest. The observation that such mutants can continue DNA synthesis and nuclear division while bud emergence is blocked (Hartwell et al., 1973(Hartwell et al., , 1974 suggests that the nuclear cycle is not dependent on the cytoplasmic processes involved in budding. Conversely, experiments with a variety of other mutations and inhibitors suggest that bud emergence is not dependent on the nuclear cycle (Hartwell et al., 1974;Pringle and Hartwell, 1981). Thus, it appears that many of the events of the yeast cell cycle are organized into two parallel and indepen-A. E. M. Adams' present address is

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Herpesviruses, a large family of double-stranded DNA enveloped viruses, accomplish infection of their host cells through viral membrane fusion with either the plasma membrane or endocytic vesicle membranes. Efficient herpesvirus infection of cells requires the concerted effort of multiple glycoproteins and involves multiple host receptors, making it a remarkably complex system of viral fusion relative to the majority of enveloped viruses, which generally require only one or two viral glycoproteins. The structures of the major glycoproteins and receptors involved in the entry of the prototypical herpesviruses herpes simplex virus (HSV) and Epstein-Barr virus (EBV) are now known. These structural studies have accelerated our understanding of HSV and EBV binding and fusion by revealing conformational changes that occur upon receptor binding, depicting potential sites of functional protein and lipid interactions, and identifying the likely viral fusogen.

Epstein-Barr virus (EBV) establishes a persistent latent infection in peripheral B lymphocytes in humans and is associated with a variety of malignancies and proliferative disorders. Latent membrane protein 2A (LMP2A) is one of only two viral proteins expressed in latently infected B lymphocytes in vivo. LMP2A blocks B cell receptor (BCR) signal transduction in vitro by binding the Syk and Lyn protein tyrosine kinases. To analyze the significance of LMP2A expression in vivo, transgenic mice with B cell lineage expression of LMP2A were generated. LMP2A expression results in the bypass of normal B lymphocyte developmental checkpoints allowing immunoglobulin-negative cells to colonize peripheral lymphoid organs, indicating that LMP2A possesses a constitutive signaling activity in nontransformed cells.