SummaryExtensive searches have so far failed to identify functional plant homologues of the mammalian apoptotic machinery. Here we report the isolation and characterisation of an Arabidopsis thaliana homologue of human Bax Inhibitor-1, AtBI-1, isolated during a differential screen of plants challenged with the phytopathogen Pseudomonas syringae. AtBI is a member of a small gene family in Arabidopsis, members of which display extensive amino acid identity to human BI-1. AtBI-1 is also functionally similar to BI-1 in its ability to suppress the lethal phenotype in yeast conferred by expression of the mammalian proapoptotic protein, Bax. Expression of AtBI-1 is rapidly upregulated in plants during wounding or pathogen challenge, suggesting a role in responses to biotic and abiotic stress. AtBI-1 upregulation appears R gene independent and is not markedly affected by mutations required for speci®c classes of R genes. However, the accumulation of AtBI-1 message is signi®cantly reduced in coi1, in which defence responses to insects, pathogens and wounding are compromised.

SummaryChanges in transcription in leaves of Arabidopsis thaliana were characterised following challenge with strains of Pseudomonas syringae pv. tomato DC3000 allowing differentiation of basal resistance (hrpA mutants), gene-specific resistance (RPM1-specified interactions) and susceptibility (wild-type pathogen). In planta avirulence gene induction, changes in host [Ca 2þ ] cyt and leaf collapse were used to delineate the transition from infection to induced resistance. The plant responds rapidly, dynamically and discriminately to infection by phytopathogenic bacteria. Within the first 2 h host transcriptional changes are common to all challenges indicating that Type III effector function does not contribute to early events in host transcriptome re-programming. The timing of induction for specific transcripts was reproducible, hierarchical and modulated at least in part through EDS1 function. R gene-specific transcripts were not observed until 3 h after inoculation. Intriguingly, the R gene-specific response proteins are expected to localise to diverse cellular addresses indicative of a global impact on cellular homeostasis. The altered transcriptional response rapidly manifests into initial symptoms of leaf collapse within 2 h, although establishment of the full macroscopic HR occurs significantly later.

Gna1, a gene encoding a Galpha subunit, a key component of signal transduction pathways, has been cloned and characterized in the wheat pathogen Stagonospora nodorum. Analysis of Gna1 expression during infection revealed a slight decrease in transcript levels shortly after germination, after which levels steadily increased until sporulation. Inactivation of Gna1 had a pleiotropic effect on phenotype. The Gna1 mutants were less pathogenic, attributed to coinciding with a defect in direct penetration. Also, Gna1 mutants were unable to sporulate, showed an albino phenotype, and secreted one or more brown pigments into growth media. Analysis of growth medium identified tyrosine, phenylalanine, and dihydroxyphenylalanine (L-DOPA) were excreted by the Gna1 strains but not by wild type. The presence of these compounds, and the insensitivity of melanization to tricyclazole suggest that S. nodorum synthesizes melanin via the L-DOPA pathway, the first fungal phytopathogen described to do so. Decreases in protease (and several other depolymerases) activities and sensitivity to osmotic stress were other phenotypes identified in the Gna1 mutants. Gna1 is the first signal transduction gene to be cloned and characterized from S. nodorum and its inactivation has uncovered several previously unknown facets of pathogenicity.

Phospholipase D (PLD; EC 3.1.4.4) has been linked to a number of cellular processes, including Tran membrane signaling and membrane degradation. Four PLD genes (alpha, beta, gamma1, and gamma2) have been cloned from Arabidopsis thalami. They encode isoforms with distinct regulatory and catalytic properties but little is known about their physiological roles. Using cDNA amplified fragment length polymorphism display and RNA blot analysis, we identified Arabidopsis PLDgamma1 and a gene encoding a lysophospholipase (EC 3.1.1.5), lysoPL1, to be differentially expressed during host response to virulent and avirulent pathogen challenge. Examination of the expression pattern of phospholipase genes induced in response to pathogen challenge was undertaken using the lysoPL1 and gene-specific probes corresponding to the PLD isoforms a, beta, and gamma1. Each mRNA class exhibited different temporal patterns of expression after infiltration of leaves with Pseudomonas syringae pv. tomato with or without avrRpm1. PLDalpha was rapidly induced and remained constitutively elevated regardless of treatment. PLDbeta was transiently induced upon pathogen challenge. However, mRNA for the lysoPL1 and PLDgamma1 genes showed enhanced and sustained elevation during an incompatible interaction, in both ndr1 and overexpressing NahG genetic backgrounds. Further evidence for differential engagement of these PLD mRNA during defense responses, other than gene-for-gene interactions, was demonstrated by their response to salicylic acid treatment or wounding. Our results indicate that genes encoding lysoPL1, PLDgamma1, and PLDbeta are induced during early responses to pathogen challenge and, additionally, PLDyl and lysoPL1 are specifically upregulated during gene-for-gene interactions, leading to the hypersensitive response. We discuss the possible role of these genes in plant-pathogen interactions.

The terms oral lichenoid reactions or oral lichenoid lesions refer to lesions histologically and clinically similar to oral lichen planus, though with the particularity that in these cases the underlying cause is identifiable. In addition, these lesions are described according to the causal factor involved, including alterations resulting from direct contact with dental restoration materials, drug-related lesions, and lesions associated to graft-versus-host disease. Drug-induced oral lichenoid reactions or oral lichenoid lesions were first cited in 1971 by Almeyda and Levantine. Since then, many drug substances have been associated with such lesions. The most common agents are nonsteroidal antiinflammatory drugs and angiotensin converting enzyme inhibitors. Key words: Oral lichenoid reactions, oral lichenoid lesions, drugs, medicines, drug-induced oral lesions.Serrano-Sánchez P, Bagán JV, Jiménez-Soriano, Sarrión G. Druginduced oral lichenoid reactions. A literature review. J Clin Exp Dent. 2010;2(2):e71-5.

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The estimated incidence of complications associated with cocaine abuse is 4.8%. Palatal perforation is a very infrequent condition within the range of complications associated with cocaine abuse. No epidemiological characteristics relating to patient age or gender have been established, and the diagnosis of the disorder requires a detailed clinical history, including antecedents of cocaine abuse. The clinical and radiological studies show palatal bone erosion and perforation of the soft or hard palate. The present study describes five cases of palatal perforation secondary to inhaled cocaine abuse. As a result of the increase in cocaine use in recent years, particularly among young adults, clinicians must be alerted to the need to include this condition when establishing a differential diagnosis.Key words: Cocaine, palatal perforation, inhalation, oronasal communication.

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