Inheritance of early blight resistance in diploid potatoes

Early blight (Alternatia solani) is a fungal disease in hot and humid environments, which causes leaf, stem and tuber lesions. Early blight resistance should be incorporated into potato cultivars because the fungicide spraying is an expensive solution for developing countries. The diploid cultivated species Solanum tuberosum group Phureja and group Stenotomum are sources of resistance alleles. The elucidation of the inheritance for early blight resistance must help to decide what could be the best breeding procedure to improve this diploid germplasm and transfer the resistance to the tetraploid level. Three experiments were carried out under controlled and field conditions to determine the heritability of this trait using nested and diallel mating designs with haploid, species and haploid-species hybrids. The narrow-sense heritability estimates were relatively high (0.64–0.78). This means that additivity was the most important type of gene action for determining resistance to early blight at the diploid level. The results suggested that diploid parents showing highest levels of resistance, throughout the cycle of disease development, can be used in 4x×2x crosses to obtain resistant tetraploid progenies to this fungal disease.     

Role of adaptor TRIF in the MyD88-independent toll-like receptor signaling pathway

Stimulation of Toll-like receptors (TLRs) triggers activation of a common MyD88-dependent signaling pathway as well as a MyD88-independent pathway that is unique to TLR3 and TLR4 signaling pathways leading to interferon (IFN)-beta production. Here we disrupted the gene encoding a Toll/IL-1 receptor (TIR) domain-containing adaptor, TRIF. TRIF-deficient mice were defective in both TLR3- and TLR4-mediated expression of IFN-beta and activation of IRF-3. Furthermore, inflammatory cytokine production in response to the TLR4 ligand, but not to other TLR ligands, was severely impaired in TRIF-deficient macrophages. Mice deficient in both MyD88 and TRIF showed complete loss of nuclear factor kappa B activation in response to TLR4 stimulation. These findings demonstrate that TRIF is essential for TLR3- and TLR4-mediated signaling pathways facilitating mammalian antiviral host defense.     

Phylogenetic analysis of Theileria sp. from sika deer, Cervus nippon, in Japan

The 18S rRNA genes of Theileria species detected in sika deer, Cervus nippon centralis in Yamaguchi and Cervus nippon yesoensis in Hokkaido, were analyzed. The percent identities of the nucleotide sequences of Theileria from Cervus nippon centralis and Cervus nippon yesoensis were more than 99%. The percent identities of the Theileria sp. from sika deer and Theileria sergenti, Theileria buffeli and Theileria cervi were 97, 96 and 95%, respectively. Phylogenetic analysis of the gene sequences also revealed that Theileria sp. detected from sika deer comprise a clade that is clearly distinct from the clade comprised of Theileria from cattle.