The genotype and the environment influences the resulting phenotype, and it is often mistakenly thought that the genotype never changes. However, the field of molecular mutations has shown that phenotypic abnormalities sometimes alter the sequence of the genetic code. Chemical mutations cause substitutions and deletions in base pairs and frameshift mutations that generate gaps in DNA during replication. Other types of mutations can cause the spontaneous loss in nitrogenous bases (lesions) in the intact double-helical DNA molecule before replication, thus altering the organisms genetic code. The following are examples of the effect of the environment on both the phenotype and the genotype:
Ultraviolet and high energy radiation (X-rays, gamma rays, and cosmic irradiation) and chemo-toxins penetrate the phenotype that in turn cause genetic mutations. Pathological viruses enter the phenotype causing a nucleotide change in the host's DNA that is then responsible for mutations within the genome: viruses are often the "precore mutants" that disrupt the base pair in the pregenome.
Many studies have indicated that aging phenotypes produce degraded gametes. In other words, increased birth defects are associated with older couples having children due to the resulting degradation in both the egg and the sperm.
Another good example is mercury poisoning. Among other abnormalities, it causes purine and pyrimidine metabolism errors and mitochondrial disturbances that lead to autism. There then occurs a "90% concordance in monozygotic twins and a 3-5% risk of autism in siblings of affected probands, a rate 50 to 100 times higher than would be expected in the general population." http://www.autismwebsite.com/ari/vaccine/mercurylong.htm
http://www.cqs.com/autismmercury.htm
Biochemical phenotype deficiencies in phenylaline (phenylalanine hydroxylase -PAH) causes lower IQ and is then genetically transmitted causing further mutations. This disorder is referred to as maternal phenylketonuria (PKU): "Phenotypic variability of PAH deficiency is correlated directly with allelic heterogeneity at the PAH locus." http://pediatrics.aappublications.org/cgi/content/full/104/2/258
Levels in certain enzymes can also lead to mutations by degenerating proteins. For example, abnormal levels in angiotensin converting enzyme (ACE) affects polymerized nucleotides before polymerase.
Ultraviolet and high energy radiation (X-rays, gamma rays, and cosmic irradiation) and chemo-toxins penetrate the phenotype that in turn cause genetic mutations. Pathological viruses enter the phenotype causing a nucleotide change in the host's DNA that is then responsible for mutations within the genome: viruses are often the "precore mutants" that disrupt the base pair in the pregenome.
Many studies have indicated that aging phenotypes produce degraded gametes. In other words, increased birth defects are associated with older couples having children due to the resulting degradation in both the egg and the sperm.
Another good example is mercury poisoning. Among other abnormalities, it causes purine and pyrimidine metabolism errors and mitochondrial disturbances that lead to autism. There then occurs a "90% concordance in monozygotic twins and a 3-5% risk of autism in siblings of affected probands, a rate 50 to 100 times higher than would be expected in the general population." http://www.autismwebsite.com/ari/vaccine/mercurylong.htm
http://www.cqs.com/autismmercury.htm
Biochemical phenotype deficiencies in phenylaline (phenylalanine hydroxylase -PAH) causes lower IQ and is then genetically transmitted causing further mutations. This disorder is referred to as maternal phenylketonuria (PKU): "Phenotypic variability of PAH deficiency is correlated directly with allelic heterogeneity at the PAH locus." http://pediatrics.aappublications.org/cgi/content/full/104/2/258
Levels in certain enzymes can also lead to mutations by degenerating proteins. For example, abnormal levels in angiotensin converting enzyme (ACE) affects polymerized nucleotides before polymerase.