Resistance to barley scald (Rhynchosporium secalis) in the Ethiopian donor lines 'Steudelli' and 'Jet', analyzed by partial least squares regression and interval mapping.

The resistance of barley (Hordeum vulgare L.) to Rhynchosporium secalis (scald) has been investigated in two crosses between the susceptible cv. 'Ingrid' and two resistant Ethiopian landraces, 'Steudelli' and 'Jet'. Doubled haploids were inoculated in replicated tests using two isolates of R. secalis, '4004' and 'WRS1872'. Expression of resistance differed widely between replicated tests. AFLP, SSR and RFLP markers were used to develop chromosome maps. Results have been analysed using partial least squares regression (PLSR) and interval mapping. In PLSR the major covariance structures or 'latent variables' between X (markers) and Y (isolates, tests) are modelled as principal components and their optimal number determined by cross-validation. In 'Steudelli' two QTL were detected, one on each of chromosomes 3H and 7H, in 4 out of 5 tests, while in 'Jet' only one (different) allele at the 3H locus was found. The validated R(2) varied between 11.0% and 64.9% in the replicated tests with '4004'.With isolate 'WRS1872' the 7H locus and another 3H locus were detected. By interval mapping the QTL detected were less stable and generally gave lower R(2) values than PLSR. PLSR does not depend on maps, but interval mapping based on values predicted by PLSR had R(2) around 90%. It is suggested that PLSR may be a useful tool in QTL analysis.

Productive infection of cerebellar granule cell neurons by JC virus in an HIV+ individual.

BACKGROUND: In the setting of severe immunosuppression, the polyomavirus JC (JCV) can cause a lytic infection of oligodendrocytes. This demyelinating disease of the CNS white matter (WM) is called progressive multifocal leukoencephalopathy (PML). JCV has a very narrow host-cell range and productive infection of neurons has never been demonstrated. Patient, methods, and results: An HIV-1-infected patient presented with signs of pyramidal tract and cerebellar dysfunction. Brain MRI revealed T2 hyperintensities in the WM of both frontal lobes and cerebellar atrophy. His disease progressed despite therapy and he died 6 months later. In addition to classic PML findings in the frontal lobe WM, autopsy revealed scattered foci of tissue destruction in the internal granule cell layer (IGCL) of the cerebellum. In these foci, enlarged granule cell neurons identified by the neuronal markers MAP-2 and NeuN reacted with antibodies specific for the polyomavirus VP1 capsid protein. Electron microscopy showed 40 nm viral particles, consistent with polyomaviruses, in these granule cell neurons. In addition, JCV DNA was detected by PCR after laser capture microdissection of cells from the areas of focal cell loss. Finally, in situ hybridization studies demonstrated that many granule cell neurons were infected with JCV but did not contain viral proteins. Sequence analysis of the JCV regulatory region from cerebellar virions showed a tandem repeat pattern also found in PML lesions of the frontal lobe WM. CONCLUSION: JCV can productively infect granule cell neurons of the IGCL of the cerebellum. This suggests a role for JCV infection of neurons in cerebellar atrophy occurring in HIV-infected individuals.

Alternative strategies in fungal race-specific parasitism.

Based on the gene-for-gene relation in race-specific resistance versus virulence, racial complexity of a pathogen population can be revealed by using host lines each with a single gene for resistance as detector. Such inventories of cereal rusts have shown: i. Genes for virulence may have pleiotropic effects acting on general fitness and their relative prevalence. ii. Genes for virulence are, as most other genes, dependent on genetic background for their general fitness. iii. Specific and general gene erosion in a pathogen population submitted to the assortative function of a race-specific host selection pressure is proportional to the degree of existing recombination and thus ultimately upon mode of reproduction (sexual or asexual). iv. Genetic storage capacity is dependent on ploidy constitution. v. Host alternation for safe annual survival favours a genetic system able to store temporarily unnecessary genes for virulence. - Due to shifting circumstances, pathogens like rusts will even inside the same forma specialis show different strategies. The trend may lead to a process of stabilizing selection and dependence on immediate and provisional flexibility just as typical of true haploids. It may lead to a pattern of preparedness: i.e. accumulation of 'unnecessary' genes for virulence. In the latter case, the modern concept of gene diversification in breeding for disease resistance is less effective. In the former case, gene accumulation can also work.