Cucurbita moschata, a cucurbit species responsive to inductive short-day (SD) photoperiods, and Zucchini yellow mosaic virus (ZYMV) were used to test whether long-distance movement of FLOWERING LOCUS T (FT) mRNA or FT is required for floral induction. Ectopic expression of FT by ZYMV was highly effective in mediating floral induction of long-day (LD)-treated plants. Moreover, the infection zone of ZYMV was far removed from floral meristems, suggesting that FT transcripts do not function as the florigenic signal in this system. Heterografting demonstrated efficient transmission of a florigenic signal from flowering Cucurbita maxima stocks to LD-grown C. moschata scions. Real-time RT-PCR performed on phloem sap collected from C. maxima stocks detected no FT transcripts, whereas mass spectrometry of phloem sap proteins revealed the presence of Cm-FTL1 and Cm-FTL2. Importantly, studies on LD-and SD-treated C. moschata plants established that Cmo-FTL1 and Cmo-FTL2 are regulated by photoperiod at the level of movement into the phloem and not by transcription. Finally, mass spectrometry of florally induced heterografted C. moschata scions revealed that C. maxima FT, but not FT mRNA, crossed the graft union in the phloem translocation stream. Collectively, these studies are consistent with FT functioning as a component of the florigenic signaling system in the cucurbits.

Mutations leading to the alteration of cellcycle checkpoint functions are a common feature of most cancers. Because of the highly regulated nature of the cell cycle, it seems likely that variation in gene dosage of key components due to functional regulatory polymorphisms could play an important role in cancer development. Here we provide evidence of the involvement of promoter single-nucleotide polymorphisms (pSNPs) in the cyclin-dependent-kinase inhibitor genes CDKN2A, CDKN2B, CDKN1A, and CDKN1B in the etiology of childhood pre-B acute lymphoblastic leukemia (ALL). A case-control study, conducted in 240 patients with pre-B ALL and 277 healthy controls, combined with a family-based analysis using 135 parental trios, all of FrenchCanadian origin, were used to evaluate single-site genotypic as well as multilocus haplotypic associations for a total of 10 pSNPs. Using both study designs, we showed evidence of association between variants CDKN2A ؊222A, CDKN2B ؊593A, and CDKN1B ؊1608A, and an increased risk of ALL. These findings suggest that variable expression levels of cell-cycle inhibitor genes CDKN2A, CDKN2B, and CDKN1B due to regulatory polymorphisms could indeed influence the risk of childhood pre-B ALL and contribute to carcinogenesis. (Blood. 2007;109:683-692)

Alfalfa mosaic virus (AlMV) coat protein is involved in systemic infection of host plants, and a specific mutation in this gene prevents the virus from moving into the upper uninoculated leaves. The coat protein also is required for different viral functions during early and late infection. To study the role of the coat protein in long-distance movement of AlMV independent of other vital functions during virus infection, we cloned the gene encoding the coat protein of AlMV into a tobacco mosaic virus (TMV)-based vector Av. This vector is deficient in long-distance movement and is limited to locally inoculated leaves because of the lack of native TMV coat protein. Expression of AlMV coat protein, directed by the subgenomic promoter of TMV coat protein in Av, supported systemic infection with the chimeric virus in Nicotiana benthamiana, Nicotiana tabacum MD609, and Spinacia oleracea. The host range of TMV was extended to include spinach as a permissive host. Here we report the alteration of a host range by incorporating genetic determinants from another virus.The interaction between virus and plant proteins determines the capability of the virus to multiply and systemically infect the host plant (1). Systemic infection with plant viruses requires cell-to-cell and long-distance movement of viral genomic RNA (2, 3). Many plant viruses find access into cells through wounds. Upon initial entry into a plant cell, the virus multiplies and moves locally from cell to cell (local infection). In most cases, the transfer of viral RNA between cells is supported by a virus-encoded movement protein(s) (4-7), whereas in some viruses the capsid protein is a primary determinant of cell-to-cell movement (8-10). The movement protein interacts with the plasmodesmata and transfers the viral RNA into a neighboring uninfected cell (11-13). During systemic infection, the virus moves through the vascular system and multiplies in upper uninoculated leaves. Movement into the upper uninoculated tissue is a critical step in the infection by many plant viruses, and prevention of this step can result in significant protection of the host(s) from virus invasion (14). Coat proteins (CPs) of several plant viruses are essential for long-distance movement (15-23). Moreover, some RNA plant viruses, such as tobacco mosaic virus (TMV) (16,17,24), cowpea mosaic virus (25), alfalfa mosaic virus (AlMV) (18), tobacco etch potyvirus (26), and red clover necrotic mosaic virus (27) require functional CP for long-distance movement.Here, to study the role of AlMV CP in long distance movement, we designed a hybrid virus consisting of TMV, the type member of the tobamovirus group, and the CP of AlMV. The TMV genome consists of a single plus-sense RNA (6,395 nt) encapsidated with a 17.5-kDa CP, which results in rodshaped particles (300 nm in length). In addition to CP, TMV has three nonstructural proteins. Proteins (183 and 126 kDa) are translated from genomic RNA and are required for virus replication (28). The 30-kDa protein is a movement protein and pro...

Understanding genetic variation might reveal the cause of individual susceptibility to a variety of complex diseases such as asthma, diabetes, and cancer. Current efforts to identify functional DNA variants have essentially been oriented toward single nucleotide polymorphisms (SNPs) found in coding regions of candidate genes since they have direct impact on the structure and function of the affected proteins. Abnormal expression of finely regulated genes could also lead to disequilibria in different metabolic pathways and/or biological processes. Thus investigation of SNPs in the promoter regions (pSNPs) of genes should improve our knowledge of the etiology of complex diseases. Unfortunately, little is known about the nature and the prevalence of pSNPs. We have analyzed 197 genes targeting the promoter region, arbitrarily defined as a 2-kb genomic segment upstream of the transcription initiation site, by screening by dHPLC for the presence of SNPs in a worldwide panel of 40 individuals. As a result 1838 pSNPs were detected, 75% of which modify (by either gain or loss) putative binding sites of known transcription factors. We also examined the distribution of these pSNPs among features such as conserved regions, repeats, and dinucleotides as well as Gene Ontology terms. This report supports the functional relevance of several of the pSNPs investigated and suggests a putative impact on disease susceptibility.