front 1 spell DNA | back 1 deoxyribonucleic acid |
front 2 F. Griffith | back 2 In 1928, F. Griffith was working with two strains of Streptococcus pneumoniae. When he mixed the remains of heat-killed pathogenic bacteria with harmless bacteria, some bacteria were changed into disease-causing bacteria. These bacteria incorporated external genetic material in a process called transformation, which results in a change in genotype and phenotype. Scientists later determined that DNA was the molecule that transformed bacteria. |
front 3 proposed a double-helical model for the structure of deoxyribonucleic acid (who)(when) | back 3 James Watson, Francis Crick; 1953 |
front 4 heritable factors (who) | back 4 Gregor Mendel |
front 5 genes on chromosomes (who) | back 5 Thomas Hunt Morgan |
front 6 DNA replication | back 6 The process by which a DNA molecule is copied |
front 7 2 chemical components of chromosomes | back 7 DNA and protein |
front 8 pathogenicity (when)(who)(how) | back 8 1928; Frederick Griffith; while trying to develop a vaccine against pneumonia. He was studying the bacterium streptococcus pneumoniae. Concluded that living nonpathogenic R bacteria had been transformed into pathogenic S bacteria by an unknown, heritable substance from the dead S cells that enabled the R cells to make capsules. |
front 9 streptococcus pneumoniae | back 9 bacterium that causes pneumonia in mammals |
front 10 pathogenic | back 10 disease-causing bacterium |
front 11 nonpathogenic | back 11 harmless bacterium |
front 12 transformation | back 12 a change in genotype and phenotype due to the assimilation of external DNA by a cell |
front 13 identified the transforming substance to be DNA (who) | back 13 Oswald Avery, Maclyn McCarty, and Colin Macleod |
front 14 virus | back 14 consist of DNA (or sometimes RNA) contained in a protein coat. The reproduce by infecting a cell and take over the cell's metabolic machinery |
front 15 bacteriophage | back 15 viruses that infect bacteria |
front 16 A. Hershey and M. Chase | back 16 In 1952, A. Hershey and M. Chase showed that DNA was the genetic material of a phage known as T2 that infects the bacterium Escherichia coli. Hershey and Chase devised an experiment using radioactive isotopes to determine whether it was a phage's DNA or protein that entered the bacteria and served as the genetic material of T2 phage. They grew T2 with radioactive sulfur to tag phage proteins and radioactive phosphorus to tag phage DNA. After infecting separate samples of E. coli with differently labeled T2 cells, they blended and centrifuged the samples to isolate the bacterial cells from the lighter viral particles. In the protein sample, radioactivity was found in the liquid and did not enter the bacterial cells. In the DNA sample, most of the radioactivity was found in the bacterial cell pellet. They concluded that viral DNA is injected into the bacterial cells and serves as the hereditary material for viruses. |
front 17 E. Chargaff | back 17 In 1950, E. Chargaff noted that the percentages of the four nitrogenous bases in DNA were species specific. He also determined that the number of A and T was approximately equal as well as the G and C. |
front 18 Chargaff's rules | back 18
|
front 19 DNA nucleotide | back 19 Phosphate, Sugar (deoxyribose), Nitrogenous base (GCAT) |
front 20 DNA structure | back 20 pg. 117 study guide |
front 21 Guanine | back 21 no data |
front 22 Cytosine | back 22 no data |
front 23 Adenine | back 23 no data |
front 24 Thymine | back 24 no data |
front 25 double helix | back 25 the presence of two strands |
front 26 antiparallel | back 26 sugar-phosphate backbone subunits run in opposite directions |
front 27 phosphodiester bond | back 27 the bond between the phosphate group and the sugar in a polynucleotide moleucle |
front 28 hydrogen bond | back 28 the bond between the nitrogenous bases that hold the strands together |
front 29 semiconservative model | back 29 the two strands of the parental molecule separate, and each functions as a template for synthesis of a new, complementary strand |
front 30 conservative model | back 30 the two parental strands reassociate after acting as templates for new strands, thus restoring the parental double helix |
front 31 dispersive model | back 31 all four strands of DNA following replication have a mixture of old and new DNA |
front 32 origins of replication | back 32 site where replication of a chromosome begins |
front 33 the E. coli chromosome, like many other bacterial chromosomes, is circular and has a single origin | back 33 no data |
front 34 a eukaryotic chromosome may have hundreds or even a few thousand replication origins | back 34 no data |
front 35 replication fork | back 35 a Y-shpaed region at the end of a replication bubble where the parental strands of DNA are being unwound |
front 36 helicases | back 36 enzyme that unwinds the helix and separates the parental strands at each replication fork. |
front 37 single-strand binding proteins | back 37 keep the separated strands apart while they serve as templates. |
front 38 topoisomerase | back 38 breaks, swivels, and rejoins the parental DNA ahead of the replication fork, relieving the strain caused by unwinding |
front 39 Primase | back 39 enzyme that joins about 5-10 RNA nucleotides base-paired to the parental strand to form the Primer needed to start the new DNA strand. |
front 40 DNA polymerases | back 40 connect nucleotides to the growing end of a new DNA strand |
front 41 A nucleotide lines up with its complementary base on the template strand; it loses two phosphate groups, and thy hydrolysis of this pyrophosphate to two inorganic phosphates provides the energy for polymerization. | back 41 no data |
front 42 DNA polymerase III | back 42 no data |
front 43 DNA polymerase I | back 43 replaces the RNA primer with DNA nucleotides |
front 44 DNA ligase | back 44 enzyme that joins the sugar-phosphate backbones of the fragments |
front 45 Initial pairing errors in nucleotide placement may occur as often as 1 per 100,000 base pairs | back 45 no data |
front 46 mismatch repair | back 46 other enzymes remove and replace incorrectly paired nucleotides that have resulted from replication errors (colon cancer) |
front 47 nucleotide excision repair | back 47 the damaged strand is cut out by a nucleases and the gap is correctly filled through the action of a DNA polymerase and ligase. |
front 48 nuclease | back 48 DNA-cutting enzyme |
front 49 nucleotide excision in skin cells | back 49 in skin cells, nucleotide excision repair frequently corrects thymine dimers caused by ultraviolet rays in sunlight. |
front 50 xeroderma pigmentosum | back 50 inherited defect in a nucleotide excision repair enzyme. Individuals with this disorder are hypersensitive to sunlight, if mutations in skin cells are left untreated, skin cancer results. |
front 51 telomeres | back 51 multiple repetitions of a short nucleotide sequence (TTAGGG in humans) at the ends of chromosomes that protect an organism's genes from being eroded during successive DNA replications. |
front 52 Telomeres two protective functions | back 52
|
front 53 telomerase | back 53 enzyme that lengthens telomeres in germ cells but not most somatic cells. |
front 54 chromatin | back 54 in eukaryotes, each chromosome consists of a single extremely long DNA double helix associated with a large amount of protein. |
front 55 histones | back 55 small, positively charged proteins that bind tightly to the negatively charged DNA. |
front 56 nucleosome | back 56
|
front 57 linker DNA | back 57 the string between beads |