Genetics

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Genetics is the branch of biology that studies heredity and trait variation in organisms. It is concerned with how particular qualities or traits are transmitted from parents to offspring, and the molecular basis of those traits. Geneticists study genetic material (DNA) and mechanisms in attempt to determine how genes are related to variations of inherited characteristics among related or similar organisms.

Genetics research broadly encompasses anything that is inherited and having to do with information that is passed from parents to offspring. In addition to the study of heredity, organism variation, and genetic mechanisms; geneticists also study the basis and possible treatment for genetic disorders such as, Cystic fibrosis, Down syndrome, Hemophilia, or Sickle cell anemia.

The term genetics comes from the Greek word genno γεννώ which means give birth. The word genetics was first applied to describe the study of inheritance and the science of variation in 1905.

Contents

Mendel's Laws

Main Article: Mendelian inheritance

In 1866, Gregor Mendel studied the transmission of seven different pea traits by carefully test-crossing many distinct varieties of peas. Studying garden peas might seem trivial to those of us who live in a modern world of cloned sheep and gene transfer, but Mendel's simple approach led to fundamental insights into genetic inheritance, known today as Mendel's Laws. Mendel did not actually know or understand the cellular mechanisms that produced the results he observed. Nonetheless, he correctly surmised the behavior of traits and the mathematical predictions of their transmission, the independent segregation of alleles during gamete production, and the independent assortment of genes. Perhaps as amazing as Mendel's discoveries was the fact that his work was largely ignored by the scientific community for over 30 years![1]

Law of dominance

Main Article: Genetic dominance

Each trait is determined by two factors (alleles), inherited one from each parent. These factors each exhibit a characteristic dominant, co-dominant, or recessive expression, and those that are dominant will mask the expression of those that are recessive.

Law of segregation

Each of the two inherited factors (alleles) possessed by the parent will segregate and pass into separate gametes (eggs or sperm) during meiosis, which will each carry only one of the factors.

Law of independent assortment

In the gametes, alleles of one gene separate independently of those of another gene, and thus all possible combinations of alleles are equally probable.

Exceptions to Mendel's Laws

There are many examples of inheritance that appear to be exceptions to Mendel's laws. Usually, they turn out to represent complex interactions among various allelic conditions.

Co-dominant

Co-dominant alleles both contribute to a phenotype. Neither is dominant over the other. Control of the human blood type group system provides a good example of co-dominant alleles.

Pleiotropism

Pleiotropism (or pleotrophy), refers to the phenomenon in which a single gene is responsible for producing multiple, distinct, and apparently unrelated phenotypic traits, that is, an individual can exhibit many different phenotypic outcomes. This is because the gene product is active in many places in the body. An example is Marfan's syndrome, where there is a defect in the gene coding for a connective tissue protein. Individuals with Marfan's syndrome exhibit abnormalities in their eyes, skeletal system, and cardiovascular system.

Epistasis

Some genes mask the expression of other genes just as a fully dominant allele masks the expression of its recessive counterpart. A gene that masks the phenotypic effect of another gene is called an epistatic gene; the gene it subordinates is the hypostatic gene. The gene for albinism in humans is an epistatic gene. It is not part of the interacting skin-color genes. Rather, its dominant allele is necessary for the development of any skin pigment, and its recessive homozygous state results in the albino condition, regardless of how many other pigment genes may be present. Because of the effects of an epistatic gene, some individuals who inherit the dominant, disease-causing gene show only partial symptoms of the disease. Some, in fact, may show no expression of the disease-causing gene, a condition referred to as nonpenetrance. The individual in whom such a nonpenetrant mutant gene exists will be phenotypically normal but still capable of passing the deleterious gene on to offspring, who may exhibit the full-blown disease.

Multigenic

Multigenic traits result from the expression of several different genes. This is true for human eye color, in which at least three different genes are responsible for determining eye color. A brown/blue gene and a central brown gene are both found on chromosome 15, whereas a green/blue gene is found on chromosome 19. The interaction between these genes is not well understood. It is speculated that there may be other genes that control other factors, such as the amount of pigment deposited in the iris. This multigenic system explains why two blue-eyed individuals can have a brown-eyed child.

Somatic mosaicism

Somatic mosaicism is responsible for conditions where an individual has two different eye colors (i.e. brown and green). In multicellular organisms, every cell in the adult is ultimately derived from the single-cell fertilized egg. Therefore, every cell in the adult normally carries the same genetic information. However, what would happen if a mutation occurred in only one cell at the two-cell stage of development? Then the adult would be composed of two types of cells: cells with the mutation and cells without. If a mutation affecting melanin production occurred in one of the cells in the cell lineage of one eye but not the other, then the eyes would have different genetic potential for melanin synthesis. This could produce eyes of two different colors.

Penetrance

Penetrance refers to the degree to which a particular allele is expressed in a population phenotype. If every individual carrying a dominant mutant gene demonstrates the mutant phenotype, the gene is said to show complete penetrance.[2]

Genetic Inheritance

In sexually reproducing organisms, each gene in an individual is represented by two copies, called alleles—one on each chromosome pair. There may be more than two alleles, or variants, for a given gene in a population, but only two alleles can be found in an individual. Therefore, the probability that a particular allele will be inherited is 50:50, that is, alleles randomly and independently segregate into daughter cells, although there are some exceptions to this rule.

The term diploid describes a state in which a cell has two sets of homologous chromosomes, or two chromosomes that are the same. The maturation of germ line stem cells into gametes requires the diploid number of each chromosome be reduced by half. Hence, gametes are said to be haploid—having only a single set of homologous chromosomes. This reduction is accomplished through a process called meiosis, where one chromosome in a diploid pair is sent to each daughter gamete. Human gametes, therefore, contain 23 chromosomes, half the number of somatic cells—all the other cells of the body.

Because the chromosome in one pair separates independently of all other chromosomes, each new gamete has the potential for a totally new combination of chromosomes. In humans, the independent segregation of the 23 chromosomes can lead to as many as 16 to 17 million different combinations in one individual's gametes. Only one of these gametes will combine with one of the nearly 17 million possible combinations from the other parent, generating a staggering potential for individual variation. Yet, this is just the beginning. Even more variation is possible when you consider the recombination between sections of chromosomes during meiosis as well as the random mutation that can occur during DNA replication. With such a range of possibilities, it is amazing that siblings look so much alike![3]

Genetic Variability

The scientific community generally assumes that cells formed without intelligent design. Therefore, existing genetic theories have been developed by those who are not looking for mechanisms that intentionally modify genetic information. Secular scientists believes that evolution is largely the result of biochemical accidents. Although geneticists and breeders have thoroughly established that genetic recombination is responsible for the variations of plant and animal breeds, we are still taught that random mutations produced the natural varieties of species such as the finches on the Galapagos islands. This contrast between fact and teachings is the result of atheistic theoretic necessity, which must propose that random reactions unreliant upon living systems are responsible for evolution.

There are two sources of genetic variability; genetic recombination and mutation. Mutations are random, unintentional nucleotide alterations that can occur in many ways, such as by errors during replication, or by exposure to chemical mutagens. Genetic recombination, on the otherhand, is performed intentionally by cellular machinery and its products remains largely uncharacterized. Both mutation and genetic recombination can modify genes, but we are being incorrectly taught that mutation is the primary source of variability driving evolution.

Illustration of DNA showing base-pairing
Illustration of DNA showing base-pairing

Little is known about recombination, except that reactions occur between chromosomes, which alter the genome of each daughter cell so that no two offspring are ever identical. Given our level of understanding, we can not yet place a limitation on their ability to manipulate DNA. It is clear the genetic constitution of organisms is not static, and the cell's molecular machinery is altering genes and creating new alleles with each passing generation. The purpose of these reactions is clear. They occur so that organisms would be able to adapt physically and biochemically, and thereby occupy earth's broad range of habitats.

It has been recognized for decades that the differences found among offspring from the same parents were the result of recombination events during meiosis. Domestic breeds, for example, are recombinants, not mutants. These rearrangements are being performed by design to provide evolutionary potential to all organisms. Contrary to popular beliefs, evolution through recombination is not random, but is instead highly systematic. In comparison, mutations are random destructive changes that destroy information. Mutations are most typically deleterious, disruptive to genome function, and corrected by the cell when detected. Evolution truly occurs through a history of genetic recombination and natural selection, but the way it is taught, you would never know anything but mutation was involved.

Contrary to what the evolutionists teach, adaptation is the result of systematic and intentional cellular reactions. However, in contrast to typical creationist perceptions, this change is not limited to the variability originally possessed by the organism. God created a cellular machinery that is performing a level of self genetic engineering. This process is creating new information and able to modify organisms so dramatically we can frequently not recognize them as related. The physical manifestations of these reactions is hard to predict, and it is also quite possible that genetic editions are being made in direct response to environmental demands.

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