modifier gene การใช้

• IFRD1 has been identified as a modifier gene for cystic fibrosis lung disease.
• Haldane provided a fundamental, theoretical basis for the existence of modifier genes.
• Characterizing modifier gene interactions may not be the easiest approach to curing disease.
• Whether this is due to modifier genes or environmental factors remains to be established.
• For these, purposes the study of both modifier genes and oligogenes are useful.
• Whole-population approaches are another important method of demonstrating the probability of modifier gene interactions.
• For the field of modifier genes, the most important responses to Fisher s theory came from Haldane.
• Background genetic effects ( modifier genes ), epistasis, somatic variation, and environmental factors all complicate the situation.
• Methods of establishing disease heritability attributable to modifier genes can be categorized into familial studies and whole-population studies.
• This gene has been identified as a candidate for a modifier gene, accounting for the extreme variation among adrenoleukodystrophy phenotypes.
• The first step involves mutation in modifier genes that regulate a complex cluster of linked genes that cause large changes in morphology.
• A "'human disease modifier gene "'is one that alters the phenotypic expression of human genetic disease.
• This is certainly true in the case that modifier genes do not exist or functionally contribute to the disease phenotype of interest.
• While many insightful early theorists contributed to current understanding of modifier genes, emphasized here are the theories of John B . S . Haldane.
• For skilled researchers using modern techniques, each step in this process of curing human genetic disease by studying modifier gene interactions poses great challenges.
• Understanding the mechanism of disease modifier genes and oligogenic inheritance may provide unique insights into the functions of gene-gene interactions that underlie human disease.
• Thus, the first step of establishing the likelihood that modifier genes indeed exist and contribute to observed variation is crucial to this described research process.
• There are multiple modifier genes which control how much tan pigment is actually expressed and so the tan areas can range from pure white to deep red.
• In 1941, Haldane applied the genetic model of modifier genes, which originated from theories of on the evolution of dominance, to phenotypic disease variation in humans.