The Cdc25 family of protein phosphatases positively regulate the cell division cycle by activating cyclindependent protein kinases. In humans and rodents, three Cdc25 family members denoted Cdc25A, -B, and -C have been identified. The murine forms of Cdc25 exhibit distinct patterns of expression both during development and in adult mouse tissues. In order to determine unique contributions made by the Cdc25C protein phosphatase to embryonic and adult cell cycles, mice lacking Cdc25C were generated. We report that Cdc25C ؊/؊ mice are viable and do not display any obvious abnormalities. Among adult tissues in which Cdc25C is detected, its transcripts are most abundant in testis, followed by thymus, ovary, spleen, and intestine. Mice lacking Cdc25C were fertile, indicating that Cdc25C does not contribute an essential function during spermatogenesis or oogenesis in the mouse. T-and B-cell development was also found to be normal in Cdc25C ؊/؊ mice, and Cdc25C؊/؊ mouse splenic T and B cells exhibited normal proliferative responses in vitro. Finally, the phosphorylation status of Cdc2, the timing of entry into mitosis, and the cellular response to DNA damage were unperturbed in mouse embryo fibroblasts lacking Cdc25C. These findings indicate that Cdc25A and/or Cdc25B may compensate for loss of Cdc25C in the mouse.

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SummaryConstitutive expression of a gene encoding tobacco mosaic virus (TMV) coat protein (CP) in transgenic plants confers resistance to infection by TMV and related tobamoviruses. Here, we examined resistance to TMV by temporal and quantitative control of TMV Cg CP (CgCP) gene expression using a simple, methoxyfenozide-inducible system in Arabidopsis plants. By soil drenching with a commercial ecdysone agonist (Intrepid-2F/methoxyfenozide), most transgenic lines were induced from undetectable levels of gene expression to protein levels from 0.05 to 0.8% (w/w) of CgCP. This corresponds to up to four times the amount of CP produced by the constitutive cauli¯ower mosaic virus (CaMV) double 35S promoter. CgCP transcripts were induced by 700-fold, without changing the expression patterns of pathogenesis-related (PR) genes. The high level of accumulation of CgCP was suf®cient to produce large amounts of virus-like particles that accumulate in large aggregates throughout the cells. In virus challenge assays, treatment with Intrepid-2F prior to TMV infection resulted in high levels of viral resistance, while no treatment or treatment with the inducer following infection did not confer resistance. This report demonstrates chemically controlled disease resistance and con®rms the utility of the ecdysone agonist-inducible system under greenhouse conditions.

CD45, a transmembrane protein tyrosine phosphatase (PTP), can either positively or negatively regulate Src‐family protein tyrosine kinase (PTK) activity in vivo. It is proposed that TCR‐initiated signaling requires the segregation of PTP activities from the engaged TCR, based upon the differential membrane compartmentalization on the T cell surface. To test the importance of CD45 exclusion from lipid microdomains for proper TCR signaling, a chimeric molecule was generated by fusing the CD45 cytoplasmic region, which contains the PTP domains, to the amino‐terminal 12 amino acids of Lck, which target Lck to lipid microdomains. Using 3A9 T lymphocyte hybridoma (3A9H) cells whose TCR recognizes hen egg‐white lysozyme (HEL), Lck‐CD45 expression resulted in its targeting to lipid microdomains. The 3A9H cells expressing Lck‐CD45 were reduced in their responses to HEL or co‐cross‐linking of CD3 and CD4, as assessed by IL‐2 production and Ca2+ mobilization. Src‐family PTK activity associated with lipid microdomains was also decreased. These results suggest that the segregation of CD45 from proximal TCR signaling components is necessary for TCR signaling and that the targeting of CD45 PTP activity to lipid microdomains on the T cell surface results in decreased sensitivity of TCR‐mediated signaling.