Academic literature on the topic 'Incompatibility system'

In 1975, a number of genetic lines discovered in our maize genetics nursery in Ames, Iowa, showed unidirectional cross-incompatibility. Later, it was found that this unidirectional cross-incompatibility is controlled by three recessive genes. One locus (cif) controls the incompatibility reaction in the female tissue and the other two (cim1 and cim2) control the incompatibility reaction in the pollen grain. The cross is incompatible only when the female parent is homozygous recessive for the cif and the male parent is homozygously recessive for the cim1 as well as the cim2 locus. Cytological studies of this unidirectional cross-incompatibility show that the site of the incompatibility reaction occurs after the entry of the pollen tubes into the transmitting tract of the incompatible silks. Between 12 and 24 h after pollination, the incompatible pollination is characterized by the swelling and bursting of pollen tubes at the tip, after which pollen tube growth stops.Key words: maize, pollen tube, cross-incompatibility.

ABSTRACT Vegetative incompatibility is a programmed cell death reaction that occurs when fungal cells of unlike genotypes fuse. Genes defining vegetative incompatibility (het genes) are highly polymorphic, and most if not all incompatibility systems include a protein partner bearing the fungus-specific domain termed the HET domain. The nonallelic het-C/het-E incompatibility system is the best-characterized incompatibility system in Podospora anserina. Cell death is triggered by interaction of specific alleles of het-C, encoding a glycolipid transfer protein, and het-E, encoding a HET domain and a WD repeat domain involved in recognition. We show here that overexpression of the isolated HET domain from het-E results in cell death. This cell death is characterized by induction of autophagy, increased vacuolization, septation, and production of lipid droplets, which are hallmarks of cell death by incompatibility. In addition, the HET domain lethality is suppressed by the same mutations as vegetative incompatibility, but not by the inactivation of het-C. These results establish the HET domain as the mediator of cell death by incompatibility and lead to a modular conception of incompatibility systems whereby recognition is ensured by the variable regions of incompatibility proteins and cell death is triggered by the HET domain.

Abstract Recent genetic analyses have demonstrated that self-incompatibility in flowering plants derives from the coordinated expression of a system of loci. To address the selective mechanisms through which a genetic system of this kind evolves, I present a three-locus model for the origin of gametophytic self-incompatibility. Conventional models assume that a single locus encodes all physiological effects associated with self-incompatibility and that the viability of offspring depends only on whether they were derived by selfing or outcrossing. My model explicitly represents the genetic determination of offspring viability by a locus subject to symmetrically overdominant selection. Initially, the level of expression of the proto-S locus is insufficient to induce self-incompatibility. Weak gametophytic self-incompatibility arises upon the introduction of a rare allele at an unlinked modifier locus which enhances the expression of the proto-S locus. While conventional models predict that the origin of self-incompatibility requires at least two- to threefold levels of inbreeding depression, I find that the comparatively low levels of inbreeding depression generated by a single overdominant locus can ensure the invasion of an enhancer of self-incompatibility under sufficiently high rates of receipt of self-pollen. Associations among components of the incompatibility system promote the origin of self-incompatibility. Enhancement of heterozygosity at the initially neutral proto-S locus improves offspring viability through associative overdominance. Further, the modifier that enhances the expression of self-incompatibility develops a direct association with heterozygosity at the overdominant viability locus. These results suggest that the evolutionary processes by which incompatibility systems originate may differ significantly from those associated with their breakdown. The genetic mechanism explored here may apply to the evolution of other systems that restrict reproduction, including maternal-fetal incompatibility in mammals.

SUMMARY Filamentous fungi spontaneously undergo vegetative cell fusion events within but also between individuals. These cell fusions (anastomoses) lead to cytoplasmic mixing and to the formation of vegetative heterokaryons (i.e., cells containing different nuclear types). The viability of these heterokaryons is genetically controlled by specific loci termed het loci (for heterokaryon incompatibility). Heterokaryotic cells formed between individuals of unlike het genotypes undergo a characteristic cell death reaction or else are severely inhibited in their growth. The biological significance of this phenomenon remains a puzzle. Heterokaryon incompatibility genes have been proposed to represent a vegetative self/nonself recognition system preventing heterokaryon formation between unlike individuals to limit horizontal transfer of cytoplasmic infectious elements. Molecular characterization of het genes and of genes participating in the incompatibility reaction has been achieved for two ascomycetes, Neurospora crassa and Podospora anserina. These analyses have shown that het genes are diverse in sequence and do not belong to a gene family and that at least some of them perform cellular functions in addition to their role in incompatibility. Divergence between the different allelic forms of a het gene is generally extensive, but single-amino-acid differences can be sufficient to trigger incompatibility. In some instances het gene evolution appears to be driven by positive selection, which suggests that the het genes indeed represent recognition systems. However, work on nonallelic incompatibility systems in P. anserina suggests that incompatibility might represent an accidental activation of a cellular system controlling adaptation to starvation.

A heterogenic system of incompatibility is described in Coprinus bisporus which involves two alleles at two loci, in addition to the unifactorial homogenic incompatibility locus already described for this two-spored species. The patterns of non-allelic heterogenic incompatibility found in C. bisporus are used to predict those expected in species with bifactorial homogenic incompatibility. This type of heterogenic incompatibility could lead to speciation.

Quantum instruments describe outcome probability as well as state change induced by measurement of a quantum system. Incompatibility of two instruments, i. e. the impossibility to realize them simultaneously on a given quantum system, generalizes incompatibility of channels and incompatibility of positive operator-valued measures (POVMs). We derive implications of instrument compatibility for the induced POVMs and channels. We also study relation of instrument compatibility to the concept of non-disturbance. Finally, we prove equivalence between instrument compatibility and postprocessing of certain instruments, which we term complementary instruments. We illustrate our findings on examples of various classes of instruments.

When a system is assembled from components, incompatibility often occurs as a result of the assembly process. The ability to quantify incompatibility is very important for making burn-in decisions because the goal of system burn-in is to minimize the incompatibility factor. In the past, incompatibility has been only partially represented in the system prediction models because it was assumed that assembly had no effect on the components. This paper presents a more accurate model for system prediction by allowing for the possibility that, in some cases, assembly adversely affects the components. After applying a superposition of delayed renewal processes and a nonhomogeneous Poisson process for modeling times between system failures, we derive and analyze the effects of component and system burn-in on the system cost and performance. Examples are included to demonstrate how to determine optimal component and system burn-in times simultaneously based on an equivalent problem formation and nonlinear programming.

Abstract Analysis of nucleotide sequences that regulate the expression of self-incompatibility in flowering plants affords a direct means of examining classical hypotheses for the origin and evolution of this major feature of mating systems. Departing from the classical view of monophyly of all forms of self-incompatibility, the current paradigm for the origin of self-incompatibility postulates multiple episodes of recruitment and modification of preexisting genes. In Brassica, the S locus, which regulates sporophytic self-incompatibility, shows homology to a multigene family present both in self-compatible congeners and in groups for which this form of self-incompatibility is atypical. A phylogenetic analysis of S-allele sequences together with homologous sequences that do not cosegregate with self-incompatibility permits dating the change of function that marked the origin of self-incompatibility. A generalized least-squares method is introduced that provides closed-form expressions for estimates and standard errors for function-specific divergence rates and times of divergence among sequences. This analysis suggests that the age of the sporophytic self-incompatibility system expressed in Brassica exceeds species divergence within the genus by four- to fivefold. The extraordinarily high levels of sequence diversity exhibited by S alleles appears to reflect their ancient derivation, with the alternative hypothesis of hypermutability rejected by the analysis.

Self–incompatibility (SI) involves the recognition and rejection of self or genetically identical pollen. Gametophytic SI is probably the most widespread of the SI systems and, so far, two completely different SI mechanisms, which appear to have evolved separately, have been identified. One mechanism is the RNase system, which is found in the Solanaceae, Rosaceae and Scrophulariaceae. The other is a complex system, so far found only in the Papaveraceae, which involves the triggering of signal transduction cascade(s) that result in rapid pollen tube inhibition and cell death. Here, we present an overview of what is currently known about the mechanisms involved in controlling pollen tube inhibition in these two systems.