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[Plant resistance genes: molecular and genetic organization, function and evolution].

Remarkable progress is achieved now in comprehension of mechanisms that determine functioning of genes responsible for plants' phytopathogenic resistance (genes R). Cloning of great number of Monocotyledones and Dicotyledones resistance genes show that most of proteins coded by these genes have conserved amino-acid motives, which show high homology to amino-acid motives of proteins with well-designated function. Common structures for most proteins produced by genes R include nucleotide-blinding site (NBS), leucine-rich repeat (LRR), site containing homology with the cytoplasmic domains of the Drosophila Toll protein and the mammalian interleukin-1 receptor (TIR), coiled-coil structure (CC), transmembrane domain (TM), and serine/threonine proteinkinase domain (PK). They are combined within the basic classes of resistance genes proteins as follows: TIR-NBS-LRR, CC-NBS-LLRR, NBS-LRR, PK, TM-CC, LRR-TM, LRR-TM-PK. The domains of proteins produced by plant resistance genes cause specific recognition of avirulence genes products and activate signaling cascade, which gives rise to resistance reaction. Some classes of plant resistance genes probably have the same evolutionary origin as the genes that control the innate immunity of ancient animals. The evolution of plant R genes proceeds primarily by duplication and equal or unequal meiotic recombination. The research on genes R functioning besides its theoretical value is a matter of considerable practical interest for construction of plant genotypes resistant against harmful organisms. The progress in comprehension of mechanisms responsible for specificity of avirulence determinants in phytopathogenic organisms recognition makes possible the creation of artificial resistance genes.

Binding Sites↗
PubMed1992

Selective breeding for increased cholinergic function: biometrical genetic analysis of muscarinic responses.

Biometric genetic analyses of behavioral and physiologic responses known to be related to muscarinic cholinergic receptors (hypothermia, hypoactivity, inhibited avoidance, and reduced responding for water) were studied in genetic crosses and backcrosses of the Flinders sensitive line (FSL) and Flinders resistant line (FRL) of rats. The FSL rats were more sensitive to the direct muscarinic agonists, arecoline and oxotremorine, and to the indirect agonist, physostigmine, than any other group. The next most sensitive group was the F1 x FSL backcross, followed by the F2, F1, F1 x FRL backcross, and the FRL, in that order. These differences between the genetic groups could be accounted for completely by either solely additive or additive plus dominance genetic factors. When dominance genetic factors contributed to the differences among groups (6 out of 15), the F1 responded like the FRL rats. The variance of the responses measured made it impossible to obtain reliable estimates of the number of genes involved in many instances; when such estimates were possible, several genes (greater than or equal to 3) appeared to be involved. We conclude that muscarinic sensitivity in rats is under genetic control, with the greatest contribution coming from additive genetic factors. Because the FSL rat appears to be a genetic animal model of depression, the finding of several genes influencing muscarinic responses may help account for the difficulties investigators have had in locating a single major gene or biological marker for human depressive disorders.

Analysis of Variance↗