eQTL mapping in transgenic alpha-synuclein carrying Caenorhabditis elegans recombinant inbred lines.

Protein aggregation of α-synuclein (αS) is a genetic and neuropathological hallmark of Parkinson's disease (PD). Studies in the model nematode Caenorhabditis elegans suggested that variation of αS aggregation depends on the genetic background. However, which genes and genetic modifiers underlie individual differences in αS pathology remains unknown.

Punctuated Loci on Chromosome IV Determine Natural Variation in Orsay Virus Susceptibility of Strains Bristol N2 and Hawaiian CB4856.

Host-pathogen interactions play a major role in evolutionary selection and shape natural genetic variation. The genetically distinct strains, Bristol N2 and Hawaiian CB4856, are differentially susceptible to the Orsay virus (OrV). Here, we report the dissection of the genetic architecture of susceptibility to OrV infection.

Genetic Variation in Complex Traits in Transgenic α-Synuclein Strains of .

Different genetic backgrounds can modify the effect of mutated genes. Human α-synuclein () gene encodes α-synuclein, and its oligomeric complexes accumulate with age and mediate the disruption of cellular homeostasis, resulting in the neuronal death that is characteristic of Parkinson's Disease. Polymorphic variants modulate this complex pathologic mechanism.

Genetic background modifies phenotypic and transcriptional responses in a C. elegans model of α-synuclein toxicity.

Background: Accumulation of protein aggregates are a major hallmark of progressive neurodegenerative disorders such as Parkinson's disease and Alzheimer's disease. Transgenic Caenorhabditis elegans nematodes expressing the human synaptic protein α-synuclein in body wall muscle show inclusions of aggregated protein, which affects similar genetic pathways as in humans. It is not however known how the effects of α-synuclein expression in C.

Genetic variation in neurodegenerative diseases and its accessibility in the model organism Caenorhabditis elegans.

Background: Neurodegenerative diseases (NGDs) such as Alzheimer's and Parkinson's are debilitating and largely untreatable conditions strongly linked to age. The clinical, neuropathological, and genetic components of NGDs indicate that neurodegeneration is a complex trait determined by multiple genes and by the environment.

Main Body: The symptoms of NGDs differ among individuals due to their genetic background, and this variation affects the onset and progression of NGD and NGD-like states.