Genetic Markers

Terminalia trees are being over-exploited because of their medicinal and economical importance leading to loss of valuable genetic resources. For sustainable utilization and conservation, assessment of genetic diversity therefore becomes imperative. We report a comprehensive first study on estimation and analysis of genetic variation through Amplified fragment length polymorphism (AFLP), inter simple sequence repeat polymorphism (ISSR) and random amplification of polymorphic DNA (RAPD) across three species of Terminalia.

BACKGROUND: Family studies and heritability estimates provide evidence for a genetic contribution to variation in the human life span. METHODS: We conducted a genome wide association study (Affymetrix 100K SNP GeneChip) for longevity-related traits in a community-based sample. We report on 5 longevity and aging traits in up to 1345 Framingham Study participants from 330 families.

Despite evidence from family studies that there is a strong genetic influence upon exceptional longevity, relatively few genetic variants have been associated with this trait. One reason could be that many genes individually have such weak effects that they cannot meet standard thresholds of genome wide significance, but as a group in specific combinations of genetic variations, they can have a strong influence.

Bivariate survival models with discretely distributed frailty based on the major gene concept and applied to the data on related individuals such as twins and sibs can be used to estimate the underlying hazard, the relative risk and the frequency of the longevity allele. To determine the position of the longevity gene, additional genetic markers data are needed. If the action of the longevity allele does not depend on its position in the genome, these two problems can be solved separately using a two-step procedure.

Despite evidence from family studies that there is a strong genetic influence upon exceptional longevity, relatively few genetic variants have been associated with this trait. One reason could be that many genes individually have such weak effects that they cannot meet standard thresholds of genome wide significance, but as a group in specific combinations of genetic variations, they can have a strong influence.

Although a decade has passed since the genetics of schizophrenia was examined for the Schizophrenia Bulletin, the epigenetic puzzle of schizophrenia has not yielded its secrets to any scientific break-through. In this article we review a sample of the highlights relevant to enlightened genetic thinking, i.e., a broad diathesis-stressor framework with multifactorial causation assumed and with provision for the epigenetic interaction of psychosocial as well as neurobiological factors.

OBJECTIVE: Some genome-wide scans and association studies for schizophrenia susceptibility genes have yielded significant positive findings, but there is disagreement between studies on their locations, and no mutation has yet been found in any gene. Since schizophrenia is a complex disorder, a study with sufficient power to detect a locus with a small or moderate gene effect is necessary.

Bipolar disorder (BD) is a worldwide highly prevalent mental disease. This disorder has a genetic inheritance characterized by complex transmission mechanisms involving multiple genes. Many investigation strategies have been put forward in order to identify BD susceptibility genes. Linkage studies reveal markers and candidate genes for the association studies. Monoaminergic system genes and intracellular signaling pathway genes are also important candidates to be investigated in the etiology of this disorder.

Attention-deficit/hyperactivity disorder (ADHD) is highly heritable. Confirmed association has been reported for several candidate genes, including DAT1, DRD4, SNAP-25, DRD5, 5HTT, HTR1B, and DBH; however, these confer relatively small risk. Family-based linkage studies have identified a number of chromosomal regions containing potential ADHD predisposing loci, some overlapping in two or more studies, including 5p, 6q, 7p, 11q, 12q, and 17p.

BACKGROUND: CpG islands (CGIs), clusters of CpG dinucleotides in GC-rich regions, are often located in the 5' end of genes and considered gene markers. Hackenberg et al. (2006) recently developed a new algorithm, CpGcluster, which uses a completely different mathematical approach from previous traditional algorithms. Their evaluation suggests that CpGcluster provides a much more efficient approach to detecting functional clusters or islands of CpGs. RESULTS: We systematically compared CpGcluster with the traditional algorithm by Takai and Jones (2002).