Genes and regulatory sites of the "host-takeover module" in the terminal redundancy of Bacillus subtilis bacteriophage SPO1.

Early in infection of Bacillus subtilis by bacteriophage SPO1, the synthesis of most host-specific macromolecules is replaced by the corresponding phage-specific biosyntheses. It is believed that this subversion of the host biosynthetic machinery is accomplished primarily by a cluster of early genes in the SPO1 terminal redundancy. Here we analyze the nucleotide sequence of this 11.5-kb "host-takeover module," which appears to be designed for particularly efficient expression. Promoters, ribosome-binding sites, and codon usage statistics all show characteristics known to be associated with efficient function in B. subtilis. The promoters and ribosome-binding sites have additional conserved features which are not characteristic of their host counterparts and which may be important for competition with host genes for the cellular biosynthetic machinery. The module includes 24 genes, tightly packed into 12 operons driven by the previously identified early promoters PE1 to PE12. The genes are smaller than average, with half of them having fewer than 100 codons. Most of their inferred products show little similarity to known proteins, although zinc finger, trans-membrane, and RNA polymerase-binding domains were identified. Transcription-termination and RNase III cleavage sites were found at appropriate locations.

Developmental regulation of cell interactions in the Arabidopsis fiddlehead-1 mutant: a role for the epidermal cell wall and cuticle.

Although the plant epidermis serves primarily a protective role, during plant development some epidermal cells specialize, becoming competent to interact not only with pollen but also with other epidermal cells. In the former case, these interactions mediate recognition, germination, and pollen growth responses and, in the latter case, result in interorgan fusions which, most commonly, alter floral architecture in ways that are thought to promote reproductive success. In either case, all of the initial signaling events must take place across the cell wall and cuticle. In Arabidopsis, mutation of the FIDDLEHEAD gene alters the shoot epidermis such that all epidermal cells become competent to participate in both types of interactions. In fdh-1 mutants, epidermal cells manifest not only a contact-mediated fusion response but also interact with pollen. Since carpel epidermal derivatives manifest both of these properties, we postulated that fdh-1 epidermal cells were ectopically expressing a carpel-like program. In this report we demonstrate that manifestation of the fdh-1 phenotype does not require the product of the AGAMOUS gene, indicating that the phenotype is either independent of the carpel development program or that fdh-1 mutations activate a carpel-specific developmental program downstream of the AG gene. Furthermore, we demonstrate that plants bearing mutations in the fdh-1 gene show significant changes in cell wall and cuticular permeability. Biochemical analyses of the lipid composition of the crude cell wall fraction reveal that fdh-1 cell walls differ from wild-type and manifest significant changes in high-molecular-weight lipid peaks. These results suggest that cell wall and cuticular permeability may be important determinants in developmental signaling between interacting cells and implicate lipids as important factors in modulating the selectivity of the permeability barrier presented by the epidermal cell wall and cuticle.