Biology Questions!!!!! Why does co-dominance, incomplete dominance, sex linked traits, and linked genes.......

Why does co-dominance, incomplete dominance, sex linked traits, and linked genes no follow classical Mendelian genetics?





What is a mutation?





How can bacteria be genetically engineered to make human insulin?





How can the environment control gene expression?








Please help.

Biology Questions!!!!! Why does co-dominance, incomplete dominance, sex linked traits, and linked genes.......
Medelian genetics is more simple, based on the idea that each parent contributes one allele to each gene, which will be either dominant or recessive. Example: If one parent gives the allele for blue eyes, and the other parent gives an allele for brown eyes, the resulting gene in their child will be Bb (both brown and blue are carried, but Brown shows through because it is dominant).





The idea that some can be co-dominant (like how a horse with one red parent and one grey parent comes out Roan, which is a mixture of the two colors rather than choosing one color or the other do be dominant), or that whether the offspring is male or female can affect the way these gene combinations play out, is not something that Mendel considered when working with his pea plant experiments.





I have no idea about the bacteria/insulin question.





The environment can control gene expression in many ways. For example, if a child is born with the genes to be tall, but grows up malnourished, he will still be short because his cells did not have the nutrition they needed to become tall. If a child is born with the gene for very light skin, but is exposed to a lot of sun without sunscreen or other protection, his skin will become dark to protect itself from the sun (tan).





I'm assuming this is for homework. I hope this helps; however, please don't just copy and paste my answers in- that's plagiarism. Restate the idea in your own words, and come up with your own examples where possible.
Reply:Look in your textbook.
Reply:The short answer to your first answer is that life just isn't always as simple as Mendel's examples are.





Mendel started by picking easy traits to study in that they were qualitative (that is, on and off, not numerical, or quantitative), and he happened to pick 7 traits that were each controlled by only a single gene, and each of these genes was located on a different chromosome, so none of them were linked to each other.





The other thing about the traits he studied is that they only had two alleles, and that one allele was completely dominant compared to the other.





But reality is, for each trait that fits these narrow criteria, there are a thousand more that don't.





For instance, lets say an organism is heterozygous for two alleles of a gene, one of them pretty functional, and the other one isn't. If the phenotype of the organism with two working copies is indistinguishable from an organism with one working copy, then we're going to say that the working allele is completely dominant to the other one. This is the case for a lot of genes we know of, like Mendel's green and yellow peas.





But lets say that the single working copy in the heterzygote can't quite do all the work without a second copy present. Having a pink flower from red and white ones would be an example of this. We then have to say that there is incomplete dominance.





Now, if instead of a working allele and a broken allele, what if we just have two working, but different alleles, like A and B blood types. If an organisms has both alleles, they show both A and B proteins on the RBCs, and so those alleles are co-dominant.





Now, Mendel picked 7 traits to follow, and they happened to be located on 7 chromosomes. This meant that each was inherited independently of the others. This lead him to conclude that all genes were inherited independently of each other, but we know now that this is wrong. Genes which are located on the same chromosomal molecule are linked, and so alleles tend to "stick" together. How well depends on how close they are physically on the chromosome. Sex linked genes are a subset of other linked genes, since those genes lie on the sex chromosomes, the alleles are "linked" to the sex of the organism.





Other people answered the mutation question; a mutation is just a change in DNA.





Bacteria can be engineered to make human insulin by giving them the DNA that codes the protein (usually by transforming them with a plasmid that has the appropriate DNA on it), and letting them crank out all the insulin they can.





The environment controls gene expression lots of ways. A couple examples can be found in bacteria; the lac operon is the classic example: the genes for eating lactose are turned off unless lactose is present, and transcription is minimal unless the cell is really hungry.





Below are a few links about the lac operon
Reply:mendels exp were on pea plants where the seven traits that he worked upon were on 4 different chromosomes.So codominance,incomplete dominance.......etc did not happen.incomplete dominance was not a pre mendalion concept because theparantals types reappear in the f2 generation.





In biology, mutations are changes to the genetic material (usually DNA or RNA). Mutations can be caused by copying errors in the genetic material during cell division and by exposure to radiation, chemicals, or viruses, or can occur deliberately under cellular control during processes such as meiosis or hypermutation. In multicellular organisms, mutations can be subdivided into germline mutations, which can be passed on to descendants and somatic mutations. The somatic mutations cannot be transmitted to descendants in animals. Plants sometimes can transmit somatic mutations to their descendents asexually or sexually (in case when flower buds develop in somatically mutated part of plant).





Mutations are considered the driving force of evolution, where less favorable (or deleterious) mutations are removed from the gene pool by natural selection, while more favorable (beneficial or advantageous) ones tend to accumulate. Neutral mutations are defined as mutations whose effects do not influence the fitness of either the species or the individuals who make up the species. These can accumulate over time. The overwhelming majority of mutations have no significant effect, since DNA repair is able to revert most changes before they become permanent mutations, and many organisms have mechanisms for eliminating otherwise permanently mutated somatic cells











the gene responsible for the production of human insulin is


fired into bacteria like e coli and they r cultured.





Gene-environment interaction is a term used to describe any phenotypic effects that are due to interactions between the environment and genes. Naive nature versus nurture debates assume that variation in a given trait is primarily due to either genes, or the individual's experiences. The current scientific view is that neither genetics nor environment are solely responsible for producing individual variation, and that virtually all traits show gene-environment interaction. The specific pattern that relates the average expression of trait across a range of environments is known as a genotype's norm of reaction.





A classic example of gene-environment interaction is Tryon's (1942) artificial selection experiment on maze-running ability in rats. Tryon produced a remarkable difference in maze running ability in two selected lines after seven generations of selecting "bright" and "dull" lines by breeding the best and worst maze running rats with others of similar abilities. The difference between these lines was clearly genetic since offspring of the two lines, raised under identical typical lab conditions, performed too differently. This difference disappeared in a single generation, if those rats were raised in an enriched environment (Cooper %26amp; Zubek 1958) with more objects to explore and more social interaction. This result shows that maze running ability is the product of a gene-by-environment interaction, the genetic effect is only seen under some environmental conditions.





The ability of an organism with a given genotype to change its phenotype in response to changes in the environment is called phenotypic plasticity. Such plasticity in some cases expresses as several highly morphologically distinct results; in other cases, a continuous norm of reaction describes the functional interrelationship of a range of environments to a range of phenotypes.





Organisms of fixed genotype may differ in the amount of phenotypic plasticity they display when exposed to the same environmental change. Hence phenotypic plasticity can evolve and be adaptive if fitness is increased by changing phenotype. Immobile organisms such as plants have well developed phenotypic plasicity giving a clue to the adaptive significance of phenotypic plasticity.





A highly illustrative example of phenotypic plasticity is found in the social insects, colonies of which depend on the division of their members into distinct castes, such as workers and guards. Individuals in separate castes differ dramatically from one another, both physically and behaviorally. However, the differences are not genetic; they arise during development and depend on the manner of treatment of the eggs by the queen and the workers, who manipulate such factors as embryonic diet and incubation temperature. The genome of each individual contains all the instructions needed to develop into any one of several 'morphs', but only the genes that form part of one developmental program are activated.





In epidemiology, a popular theory is that rising incidences of coronary heart disease and Type II diabetes in human populations undergoing industrialization is due to a mismatch between a metabolic phenotype determined in development and the nutritional environment an individual is subsequently exposed to. This is known as the 'Thrifty phenotype' hypothesis (see Evolutionary psychology).
Reply:if this is homework open your book...otherwise im waring of assisting you as these questions sound similiar to those on an exam in child development