Chromosomal+and+Molecular+Basis+of+Inheritance

=Chapter 15, 16: Chromosomal and Molecular Basis of Inheritance= By: Lauren Hales-Beck

=Chapter 15 Objectives 1-5,7,8=

[[image:multicolorstar.gif width="40" height="36"]]Related activities

 * Ch. 15 Outline: Chromosome Basis of Inheritance
 * Genetic Mapping Wkst
 * Essay Sex Chromosome Questions [|1], [|2] , [|3] , [|4] , [|5] , and [|6]

[[image:multicolorstar.gif width="37" height="34"]]Vocabulary

 * Chromosome theory of Inheritance: mendelian genes have specific loci on chromosomes, which then undergo segregation and independent assortment.
 * Wild type: phenotype most common in a natural population.
 * Mutant phenotypes: traits that are alternative to wild type.
 * Sex-linked genes: genes located on sex chromosomes X and Y.
 * Linked genes (diff. from sex-linked): genes that are passed along in a unit.
 * Genetic recombination: new combo of traits inherited form two parents. Different genotype than parent genotype.
 * Parental types: offspring inherited the same traits that the parents have.
 * Recombinants: offspring has a different combo of genotypes than the parents.
 * Genetic Map: ordered list pf the genetic loci along a particular chromosome.
 * Linkage map: genetic map based on recombination frequencies.
 * Cytological map: a map that locates genes based on chromosome features that can be seen with a microscope.
 * Duchenne muscular dystrophy: disease defined as a continuous weakening of the muscles and loss of coordination.
 * Hemophilia: disease where a person has the absence of a protein required for blood clotting.
 * Barr body: an inactive X chromosome that is not expressed, but remains active for sex cell division.
 * Nondisjuction: where pair of homologous chromosomes does not move apart during meiosis I or when sister chromatins do not separate during meiosis II.
 * Aneuploidy: abnormal chromosome number.
 * Trisomic: describes an aneuploidy with an extra chromosome.
 * Monomic: describes an aneuploidy with a missing chromosome.
 * Polyploidy: term for chromosomal alteration.
 * Deletion: when a chromosome fragment lacking a centromere is lost in cell division.
 * Duplication: the fragment joins a homologous chromosome, which produces another fragment.
 * Inversion: reattachment to the original chromosome in reverse order.
 * Translocation: fragment joins a nonhomoglous chromosome, results in a rearrangement.
 * Down syndrome: the result of an extra chromosome 21 (total of 47 chromosomes).

[[image:multicolorstar.gif width="41" height="33"]]Important Content
Led to the discovery of sex-linked genes by way of mating fruit flies. When he mated a red-eyed female with a white-eyed male, all of the offspring from the F1 generation had red eyes, but he continued on to mate a male and female from this F1 generation. What came from this mating strategy were three red-eyed offspring and one white-eyed offspring. What Morgan soon observed was that the only offspring with the white eyes was male. This is where he decided that the fly's eye color was linked to the sex of the offspring. He found that the genes had to be on the X chromosomes, which is why the females did not show the white eye phenotype. The white-eyed trait is recessive; this means that the female offspring would have to have two recessive X chromosomes to be able to have white eyes. This was genetically impossible for the females in the F2 generation to have so soon. The male was able to have white eyes because males receive one X chromosome. This X chromosome could carry the recessive gene and reveal the white phenotype because the Y chromosome cannot mask the X chromosome. Recombinants are offspring where the traits they exhibit are a different combination of their parents. An example of this comes from the good old pea experiment where the parents were yellow-round and green-wrinkled. The recombinants would be yellow-wrinkled and green-round. The offspring inherited the switched traits. There is a fly example of wing type and body color on p. 265 in the book. Recombinants are said to come from genes crossing over during meiosis. This is where nonsister chromatins swap genes on their chromosomes when they are touching. Then when they are pulled apart in metaphase I, the genes are switched from where they would regularly be. Genetic mapping used recombination data to construct a map of a chromosome. This genetic map shows where genetic loci could most likely appear on a chromosome with reference to other genes that correspond in recombination frequencies. Morgan’s reason for the map was that "the greater the distance between two genes, the more points there are between then where crossing over can occur." Recombination frequencies are determined by this distance = higher chance of crossing over.
 * Thomas Morgan Experiement
 * Genetic Recombinants

Down Syndrome: extra chromosome 21. Can be distinguished from normal males and females due to characteristic facial features. People with Down syndrome are often sterile and have mental retardation. Affects 1 in every 700 people. Monosomy X: only one X chromosome. individuals are female with sex organs that do not mature - sterile. Affect 1 out of every 5000 people. Klinefltner's Syndrome (XXY): Males, with small sex organs which are sterile and small. Have female characteristcs of brests and other female anomalites. Affect 1 out of 2000 people. Trisomy X (XXX): Females that cannot be distingushed from a normal female. Both healthy and fertile. Affects 1 in every 1000 people.
 * [|Disorders casued by non-disjuction] more on p. 273


 * • Alteration of Chromosomal Structure . . . more on page 272
 * • Alteration of Chromosomal Structure . . . more on page 272

Resources: [|Genetics and Development]

=Chapter 16 Objectives: 1-6=

[[image:multicolorstar.gif width="40" height="36"]] Related activities

 * Ch. 16 Outline: Molecular Basis of Inheritance
 * [[file:DNA overhead notes]]
 * Study Guide for ch. 16, 17, 20

[[image:multicolorstar.gif width="37" height="34"]]Vocabulary

 * Transformation (p. 279): a change in genotype and phenotype due to the assimilation of external DNA by a cell.
 * Bacteriophages (p. 279): bacteria-eaters.
 * Double Helix (p. 282): the structure of DNA with two strands.
 * Semi-conservative (p. 284): Replication form involving a parent strand and daughter strand of DNA.
 * Origins of Replication (p. 286): special sites where the replication of DNA begins.
 * Replication Fork (p. 286): Y-shaped region where new DNA strands elongate.
 * DNA polymerase (p. 286): Enzymes that catalyze elongation of new DNA.
 * Leading Strand (p. 287): DNA strand made in the 5’ to 3’ direction.
 * Lagging Strand (p. 288): make in the opposite direction than the leading strand. Has to be made in short fragments called okazaki fragments.
 * DNA ligase (p. 288): connect the okazaki fragments into one DNA strand.
 * Primer (p. 288): short amount of RNA.
 * Primase (p. 288): enzyme that joins the RNA into the primer.
 * Helicase (p. 289): enzyme that untwists the double helix.
 * Single-strand binding protein (p. 289): hold DNA apart while replication is being completed.
 * Mismatch Repair (p. 289): fixes mistakes in the new DNA.
 * Nuclease (p. 290): DNA cutting enzyme.
 * Telomeres (p. 291): at the end of DNA to protect the new DNA. Short nucleotide sequence TTAGGG.
 * Telomerase (p. 291): enzyme that catalyzes the lengthening of Telomeres.

[[image:multicolorstar.gif width="41" height="33"]]Important Content
Discovered transformation from an experiment of mice in 1928. Griffith used streptococcus pneumonia bacteria to inject into mice. There are two types of this streptococcus; smooth and rough. The smooth bacterium infects and kills the host because the body cannot break down the bacteria. The rough bacteria don't kill the host because it does not have the caplet covering that the smooth bacteria is encapsulated with. The experiments were done on four mice. In mouse (a), a smooth bacterium was injected and the mouse died. Mouse (b), rough bacteria was injected and the mouse lived. Mouse (c) smooth heat-killed bacteria were injected and the mouse also lived. The last mouse (d) was injected with smooth heat-killed and rough bacteria, the mouse once again died. Griffith took the bacteria from mouse (d) and found that the smooth bacteria transformed the living rough bacteria into smooth bacteria. Discovered the use of genetic material in 1952. Used bacteriophage to see weather a protein or DNA was responsible for reprogramming host cells to produce viruses. First they grew a T2 bacteriophage in radioactive sulfur, where the sulfur soaked into the protein. Then they grew T2 in radioactive phosphorus, where it soaked into the DNA. They then took these radioactive soaked bacteriophages and mixed them with bacteria cells. The T2 bacteriophages injected their DNA into the bacteria cells. The bacterium infected with the sulfur and phosphorus was put into a blender to shake off the phages still connected to the bacterium. Hershey and Chase then spun the bacterium in a centrifuge to separate the phages from the bacterium. The bacterium condensed down into a pellet at the bottom of the tube. Both the pellet (DNA) and supernatant (phages) were measured for radioactivity. The sulfur in the first experiment was found to be in the supernatant and not in the DNA pellet. The phosphorus was found in the DNA pellet and not the supernatant. This data concluded that "the injected DNA molecules cause the cells to produce new viral DNA and proteins." This also gave Hershey and Chase the evidence that nucleic acids, not proteins, are hereditary material. Erwin Chargaff found that the amounts of the DNA bases: adenine (A), thymine (T), guanine (G), and cytosine (C) are not all equal throughout DNA as previously thought. He found that the amount of adenine equaled thymine and guanine equaled cytosine. Human DNA is approximately 30.9% A, 29.4% T; 19.9% G, and 19.8% C. Discovered by Rosalind Franklin's x-rays crystallography the structure of DNA. They figured that DNA was helical and decided that the strand had a width of 2 nanometers with bases stacked 0.34 nanometers apart. This width suggested that DNA was double stranded; this led to the name the double helix. Watson and Crick started to make models. Eventually they had to place the bases inside the model with the backbone outside. Studying the x-rays, DNA seemed to turn every 0.34 nanometers along the length meaning that there were 10 base pairs per turn. The bases proved to be difficult. At first Watson and Crick thought that A went with A, T - T, C - C, and G - G; which wasn't the case. An A - A pair was too wide, while a T - T pair was too narrow. Finally they put A - T and C - G making it the perfect width. They also found out that the structures of A made it only compatible to T and the same was found with C and G. This information also helped Chafgaff's rules finally make sense. Watson and Crick published their report in a scientific journal in April 1953.
 * Fredrick Griffith Experiment[[image:Gen_Mat_I.png align="right"]]
 * Hershey and Chase Experiment
 * Chargaff's Rules
 * Watson and Crick discovered DNA model

DNA replicates by way of opening the parent strands and using the parent strand as a template to make daughter strands. After replication is completed, there are two identical DNA models. They each consist of a parent strand and a daughter strand. This is called the semi conservative model where the parent strand remains intact and a new strand made from scratch. DNA replications begin at special sites called origin of replication. At both ends of the origin of replication is a replication fork. There are two types of strands: leading and lagging. The leading strand runs 5' to 3', while the lagging strand runs 3' to 5'. The leading strand is a solid continuous strand, while the lagging is make up of Okazaki fragments. The DNA is "unzipped" by helicase and held open by single-strand binding proteins. DNA replication is begun with DNA polymerase which elongate new DNA that is synthesized on the template. The Okazaki fragments do to where RNA primer has started a section and continue it. Primase joins RNA nucleotides together to make RNA primer. DNA ligase joins two Okazaki fragments together to make a whole strand. Mismatch repair corrects all mistakes that happen during DNA replication. Any mistakes are cut out by a nuclease and the gap is filled in with DNA polymerase. The newly replicated and correct DNA is then capped with Telomeres (TTAGGG) and these telomeres are lengthened by telomerase.
 * DNA Replication



Links: [|Molecular Genetics] [|DNA Replication] need to press play when a new enzyme comes in.