The phenotypic diversity. The modificational diversity

The phenotypic diversity shows phenotype changes under environmental condition, which not affect genotype, but level of it expression is determined by genotype.

The modificational diversity. The modificational diversity describes the individual’s changes caused by environmental factors. To understand the relative impact of genotype and the environment in phenotype formation we need to investigate modification appearing under some environmental conditions. The examples are skin pigmentation of UV light, weight varying due to diet imbalance, effects of low vitamin intake, and so on. The modification diversity reaction is understandable and has only one direction to change. That means that the same environmental effect causes the same organism reaction in organisms.

This is a main difference from mutations, which have strait direction in changes. Each mutagen may cause different effects. And different mutagens may cause the same mutation. The most common modification in mammals and humans are modifications related to weight varying due to diet misbalance. The level of modification expression corresponds with intensity and duration of environmental effect. The mutations, especially genetic ones, don’t follow such pattern. The level of phenotype changes in genetic mutation don’t correspond with intensity and duration of environmental effect.

Each trait of humans are formed in genotype and phenotype interaction. And variations of traits are limited. They are limited by material matter of heredity structures, which are in appropriate limits called norm of reaction. The norm of reaction - are the limits of modificational diversity of organism. In a human we may observe a full range of traits starting from completely determined by genotype (ABO blood groups, iris color etc.) to determined with strong help of environment (human height ) and finishing by almost fully determined by environment (weight).

The modifications, in spite of mutations, are not inherited. Nevertheless, for a long time in biology the incorrect thesis of J.B. Lamark was supported. He suggested that modification might be inherited. In the end of 19th century, A. Veismann refuted arguments of J.B. Lamark. He cut off rat’s tails in 22 generations but in spite of this, rats in 23rd generation had tails.

The ontogenetic diversity. During ontogenesis many physiological, morphological, biochemical and other organism properties are being changed. Their time and place of appearance in phenotype are strictly determined by genotype. The ontogenetic diversity is diversity showing normal development changes in organism or its cells during individual development. You can recall the examples in your own individual development.

The main difference from genotypic diversity is that organisms have the same genotype throughout all individual development. From a variety of mechanisms controlling ontogenetic diversity the main are the following: different gene activity, different activity of endocrine glands, different relation between processes of growth and differentiation in different periods of life. The examples are milk- teeth exchange, development of secondary sex signs, grey hair, loosing of skin elastics, and the increased rate of bone fractures in elderly.

Ontogenetic diversity plays a definite role in the development of some hereditary diseases. A range of hereditary defects appears in embryo (polydactilia, syndactilia, achondrodisplasia, amavrotic idioty). Some are developed in childhood or puberty. And very few are developed in elderly. F or example, family F riedreich’s ataxia are developed in child 6-12 years of age, cerebellum ataxia are developed in young men 20-30 years of age, alcaptonuria - around 30 years of age, diabetes mellitus type II - 40 years of age, gout - after 40 years of age and only in men.

To treat properly, the doctor needs to know the mechanisms of ontogenetic diversity and their role in development of some hereditary human diseases. For example, phenilketonuria is hereditary effect, which may be evaluated right after birth. It is related with intolerance to one amino acid. If the patients are treated well in the first years of life they can fight with disease by themselves after puberty. But if the patients aren’t treated they develop irreversible changes in the brain.