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Cauliflower Mosaic Virus (CaMV) aphid transmissibility depends on the concomitant presence of an 18 kDa polypeptide and an intact gene II coding for this P18 protein. The molecular basis of this phenomenon can now be analyzed since the complete nucleotide sequence is known for two transmissible (S and D/H) and one non-transmissible strain (CM 1841). In order to get more detail on this topic, we have determined the nucleotide sequence of gene II and flanking regions for an additional strain PV147. The DNAs of strains CM1841 and PV147 show considerable homology (more than with strains S and D/H) but these strains have opposite phenotypes. In consequence, strain PV147 allows us to specify further the putative point mutations responsible for the lack of aphid transmission observed with CM 1841. The results obtained show that substitutions possibly involved in this defective phenotype are only two, instead of five on the basis of preexisting data. More interestingly, analysis of the potential effect of such substitutions upon predicted secondary structures of the different P18 polypeptides led us to a new hypothesis. Strain CM1841 could be mutated in the expression of gene II, a gene intact in other respects.

Cauliflower Mosaic Virus (CaMV) aphid transmissibility depends on the concomitant presence of an 18 kDa polypeptide and an intact gene II coding for this P18 protein. The molecular basis of this phenomenon can now be analyzed since the complete nucleotide sequence is known for two transmissible (S and D/H) and one non‐transmissible strain (CM 1841). In order to get more detail on this topic, we have determined the nucleotide sequence of gene II and flanking regions for an additional strain PV147. The DNAs of strains CM1841 and PV147 show considerable homology (more than with strains S and D/H) but these strains have opposite phenotypes. In consequence, strain PV147 allows us to specify further the putative point mutations responsible for the lack of aphid transmission observed with CM 1841. The results obtained show that substitutions possibly involved in this defective phenotype are only two, instead of five on the basis of preexisting data. More interestingly, analysis of the potential effect of such substitutions upon predicted secondary structures of the different P18 polypeptides led us to a new hypothesis. Strain CM1841 could be mutated in the expression of gene II, a gene intact in other respects.

pAntp, a 60 amino acid long peptide corresponding to the homeodomain of the Drosophila Antennapediaprotein, translocates through neuronal membranes when added exogenously to neurons in culture, where it accumulates in the nucleus and promotes neurite outgrowth. We proposed that the peptide, once internalized, may compete for homeoprotein DNA binding sites. To investigate this point, we have produced a permanent fibroblast cell line which carries a luciferase reporter gene under the control of a 93 bp genomic region of the HOXD9promoter with binding sites for homeoproteins. Externally added pAntp specifically down‐regulates the expression of the reporter gene, suggesting that the neurotrophic effects observed previously are mediated by direct binding of pAntp to homeoprotein target sites.