Viroids are subviral plant pathogens at the frontier of life. They are solely composed by a single-stranded circular RNA of 246–401 nt with a compact secondary structure. Viroids replicate autonomously when inoculated into their host plants and incite, in most of them, economically important diseases. In contrast to viruses, viroids do not code for any protein and depend on host enzymes for their replication, which in some viroids occurs in the nucleus and in others in the chloroplast, through a rolling-circle mechanism with three catalytic steps. Quite remarkably, however, one of the steps, cleavage of the oligomeric head-to-tail replicative intermediates to unit-length strands, is mediated in certain viroids by hammerhead ribozymes that can be formed by their strands of both polarities. Viroids induce disease by direct interaction with host factors, the nature of which is presently unknown. Some properties of viroids, particularly the presence of ribozymes, suggest that they might have appeared very early in evolution and could represent ˈliving fossilsˈ of the precellular RNA world that presumably preceded our current world based on DNA and proteins.
Plant–fungus interactions are highly diverse, either being beneficial to the host plant such as those leading to mycorhizal symbiosis, or very detrimental when leading to severe diseases. Since the beginning of agriculture, improvement of plant resistance to pathogens has remained a major challenge. Breeding for resistance, first conducted empirically in the past centuries, was then performed on a more theoretical basis after the statement of heredity laws by Mendel at the end of the XIXth century. As a result, most cultivated species contain various cultivars whose resistance or susceptibility to a given pathogen species depend on their interaction with various races of that pathogen. Such highly specific race-cultivar systems are particularly suited for understanding the molecular dialogue which underlies compatible (host susceptible/pathogen virulent) or incompatible (host resistant/pathogen avirulent) interactions. During the twentieth century, one of the major events that paved the way for future research was the statement by Flor 〚1946, 1947〛 of the gene-for-gene concept. Studying inheritance of the disease phenotype in the interaction between flax and Melampsora lini he showed that resistance in the host and avirulence in the pathogen are dictated by single dominant genes which correspond one to one, i.e. one resistance gene for one avirulence gene. The fact that incompatibility may depend on the presence of only one resistance (R) gene in the host and one avirulence (Avr) gene in the pathogen was fully confirmed about 40 years later. Molecular genetics and complementation experiments have allowed to isolate numerous R and Avr genes from various plant–pathogen systems, and to verify the gene-for-gene concept. These studies have enlightened the elicitor/receptor concept, formerly introduced to account for the specificity of the compatible and incompatible interactions. The present knowledge of R and Avr genes also allows to predict how such genes have evolved and how they could be used to improve disease resistance. At the beginning of the twenty first century, this remains a major challenge in view of the severe losses caused by pests and pathogens to most crops on the earth.
Two scientists contributed to the discovery of the first virus, Tobacco mosaic virus. Ivanoski reported in 1892 that extracts from infected leaves were still infectious after filtration through a Chamberland filter-candle. Bacteria are retained by such filters, a new world was discovered : filterable pathogens. However, Ivanovski probably did not grasp the full meaning of his discovery. Beijerinck, in 1898, was the first to call ‘virus’, the incitant of the tobacco mosaic. He showed that the incitant was able to migrate in an agar gel, therefore being an infectious soluble agent, or a ‘contagium vivum fluidum’ and definitively not a ‘contagium fixum’ as would be a bacteria. Ivanovski and Beijerinck brought unequal but decisive and complementary contributions to the discovery of viruses. Since then, discoveries made on Tobacco mosaic virus have stood out as milestones of virology history.
The eighteenth century is the beginning of the scientific emergence of plant pathology. Naturalists disproved spontaneous generation, meteorological and supernatural origins of plant diseases. It is necessary to explain plant alterations and to find possibilities of control to reduce significant losses of yield and to limit famine. In 1728, the words ‘plant parasite’,’plant disease’, and ‘epidemics’ were used for the first time. In 1755, the first seed treatment and, in 1805 the first description of a whole cycle of plant disease were proposed. In the nineteenth century much work on bunt and rusts of wheat, potato downy mildew, and grape vine powdery mildew established the scientific status of plant pathology. A retrospective analysis of these early developments shows a very good concordance with Koch’s postulate published one century later.
Some defense mechanisms of plants are of the passive type while others are induced after perception of the pathogenic microorganism (very specific gene-for-gene recognition) or of microbial components (non specific elicitors). These recognition events trigger an array of plant signals and a cascade of signalling pathways which activate a battery of metabolic alterations responsible for the observed induced resistance. These include the stimulated production of low molecular weight molecules with antibiotic activity, cell wall reinforcement by deposition and cross-linking of various macromolecules, and accumulation of a wide range of PR (‘pathogenesis-related’) proteins that exhibit direct and/or indirect antimicrobial activities. The present studies aim to caracterize natural elicitors or design chemical messengers capable of triggering an array of plant defense responses. Treatments of plants with elicitors could be an alternative strategy of crop protection with a more satisfactory preservation of the environment.
All the 〚HOAC〛 lines derived from the Pervenets mutant carry a specific RFLP (oleHOS) revealed by an oleate desaturase cDNA used as a probe. The 〚LO〛 (linoleic) genotypes do not carry oleHOS, but another allele: oleLOR. We studied 〚HOAC〛 heredity in two segregating populations. In an F2 population, the 〚HOAC〛 trait co-segregated with oleHOS. In a recombinant inbred line F6 population, all 〚HOAC〛 RI lines carried oleHOS. The RI lines carrying oleHOS were either 〚LO〛 or 〚HOAC〛. The absence of 〚HOAC〛 RI lines with oleLOR eliminated the occurrence of a recombination event between the locus carrying oleHOS and the locus carrying Pervenets allele. The 〚HOAC〛 trait is due to 2 independent loci: the locus carrying oleHOS allele and another locus. One allele at this other locus may suppress the effect of oleHOS allele on the 〚HOAC〛 trait. The existence of this suppressor allele has only been suggested for sunflower.
Effects of RU 486 (10 mg·kg–1, per.os) were assessed at mid-pregnancy in the rat. One hour after RU 486 treatment, myometrial electrical activity stayed low. It increased from the 3rd hour after administration of RU 486 and a perfect synchronization of the bursts of the action potentials was observed from the 6th h to the 24th h. Tissular steroid hormones and PGF2α, evaluated at hour 6 after RU 486 administration, showed a decrease of progesterone concentrations in both myometrium and uterus. Estradiol levels decreased in uterus whereas, PGF2α levels increased in both myometrium and uterus. These results show for the first time that RU 486 strongly increases the myometrial electrical activity in the rat at mid-pregnancy. This action was closely related to E2, P4 and PGF2α concentrations.
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