Chapter 16 Flashcards

1
Q

t. Hereditary information in DNA directs the development of

A

your biochemical, anatomical, physiological, and, to some extent, behavioral traits.

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2
Q

why did ppl not think nucleic acids cld hold genetic material

A

Moreover, little was known
about nucleic acids, whose physical and chemical properties
seemed far too uniform to account for the multitude of specific
inherited traits exhibited by every organism. This view gradually changed as the role of DNA in heredity was worked out in
studies of bacteria and the viruses that infect them, systems far
simpler than fruit flies or human

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3
Q

why did ppl think proteins held the genetic material

A
Until the 
1940s, the case for proteins seemed stronger: Biochemists 
had identified proteins as a class of macromolecules with great 
heterogeneity and specificity of function, essential requirements for the hereditary material
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4
Q

griffits experiment, what happened nd why

A

Furthermore, this newly acquired trait of
pathogenicity was inherited by all the descendants of the
transformed bacteria. Apparently, some chemical component
of the dead pathogenic cells caused this heritable change,
although the identity of the substance was not known.

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5
Q

transformtion

A

Griffith called the phenomenon transformation, now
defined as a change in genotype and phenotype due to the
assimilation of external DNA by a cell.

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6
Q

conclusion of griffith’s experiment

A

The living 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.

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7
Q

bacteriophages

A

f viruses that infect bacteria (Figure 16.3). These
viruses are called bacteriophages (meaning “bacteria-eaters”),
or phages for short

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8
Q

virus

A

A virus is little more than DNA (or sometimes RNA) enclosed
by a protective coat, which is often simply protein. To produce
more viruses, a virus must infect a cell and take over the cell’s
metabolic machinery

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9
Q

why did hershey n chase use sulfur and phosphorous and why was it incorportated into only one component

A

In their experiment, they used a radioactive isotope of sulfur
to tag protein in one batch of T2 and a radioactive isotope of
phosphorus to tag DNA in a second batch. Because protein, but
not DNA, contains sulfur, radioactive sulfur atoms were incorporated only into the protein of the phage. In a similar way,
the atoms of radioactive phosphorus labeled only the DNA,
not the protein, because nearly all the phage’s phosphorus is
in its DNA

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10
Q

what happened in hershey n chase’s experiment

A

In the experiment, separate samples of nonradioactive E. coli cells were infected with the protein-labeled and
DNA-labeled batches of T2. The researchers then tested the two
samples shortly after the onset of infection to see which type
of molecule—protein or DNA—had entered the bacterial cells
and would therefore be capable of reprogramming them.

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11
Q

result of hershey n chase

A

Results When proteins were labeled (batch 1), radioactivity
remained outside the cells, but when DNA was labeled (batch 2),
radioactivity was found inside the cells. Cells containing radioactive
phage DNA released new phages with some radioactive phosphorus.

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12
Q

conclusion of hershey n chase

A

Conclusion Phage DNA entered bacterial cells, but phage proteins
did not. Hershey and Chase concluded that DNA, not protein,
functions as the genetic material of phage T2.

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13
Q

the result of hershey n chase further showed tht… and what was concluded

A

This result further showed that the
DNA inside the cell played an ongoing role during the infection process. They concluded that the DNA injected by the
phage must be the molecule carrying the genetic information
that makes the cells produce new viral DNA and proteins. The
Hershey-Chase experiment was a landmark study because it
provided powerful evidence that nucleic acids, rather than proteins, are the hereditary material, at least for certain viruses.

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14
Q

double helix

A

. The presence of two strands accounts for

the now-familiar term double helix

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15
Q

antiparallel

A
Watson constructed such a model, shown in the small photo on the first 
page of this chapter. In this model, the two sugar-phosphate 
backbones are antiparallel—that is, their subunits run in 
opposite directions (
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16
Q

step one of dna rep

A

e parental molecule has two complementary strands of DNA. Each base is paired by
hydrogen bonding with its specific partner,
A with T and G with C.

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17
Q

step two of dna rep

A

First, the two DNA strands are separated.
Each parental strand can now serve as a
template for a new, complementary
strand.

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18
Q

step three of dna rep

A

(c) Nucleotides complementary to the parental
(dark blue) strand are connected to form the
sugar-phosphate backbones of th

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19
Q

semiconservative model

A
This semiconservative model
can be distinguished from a conservative model of replication, in which the two parental strands somehow come back 
together after the process (that is, the parental molecule is 
conserved).The two strands
of the parental
molecule separate,
and each functions
as a template for
synthesis of a new, 
complementary
strand.
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20
Q

dispersive

A
Each strand of
both daughter 
molecules contains a mixture of 
old and newly 
synthesized DNA.
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21
Q

conservative

A
The two parental
strands reassociate
after acting as
templates for new
strands, thus
restoring the
parental double
helix.
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22
Q

concl of meselsohn and stahl

A

n Meselson and Stahl compared their results to those
predicted by each of the three models in Figure 16.10, as shown
below. The first replication in the 14N medium produced a band of
hybrid (15N-14N) DNA. This result eliminated the conservative model.
The second replication produced both light and hybrid DNA, a result
that refuted the dispersive model and supported the semiconservative model. They therefore concluded that DNA replication is
semiconservative.

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23
Q

replication fork

A

At each end of a replication bubble is a replication
fork, a Y-shaped region where the parental strands of DNA
are being unwound. Several kinds of proteins participate in
the unwinding

24
Q

helicase

A

Helicases are enzymes that
untwist the double helix at the replication forks, separating the two parental strands and making them available
as template strands.

25
single-strand binding proteins
After the parental strands separate, single-strand binding proteins bind to the unpaired DNA strands, keeping them from re-pairing. The untwisting of the double helix causes tighter twisting and strain ahead of the replication fork
26
topoisomerase
Topoisomerase is an enzyme that helps relieve this strain by breaking, swiveling, and rejoining DNA strands.
27
primer
. The initial nucleotide chain that is produced during DNA synthesis is actually a short stretch of RNA, not DNA. This RNA chain is called a primer and is synthesized by the enzyme primase
28
Primase starts a
complementary RNA chain with a single RNA nucleotide and adds RNA nucleotides one at a time, using the parental DNA strand as a template. The completed primer, generally 5–10 nucleotides long, is thus base-paired to the template strand. The new DNA strand will start from the 3′ end of the RNA primer.
29
dna pols
Enzymes called DNA polymerases catalyze the synthesis | of new DNA by adding nucleotides to the 3′ end of a preexisting chain.
30
The situation in eukaryotes is more complicated, with at least 11 different DNA polymerases discovered so far, although
the general | principles are the same.
31
Like ATP, the nucleotides used for DNA synthesis are chemically reactive, partly because their triphosphate tails have an unstable cluster of negative charge. DNA polymerase catalyzes
s the addition of each monomer via a dehydration reaction (see Figure 5.2a). As each monomer is joined to the growing end of a DNA strand, two phosphate groups are lost as a molecule of pyrophosphate (
32
leading strand
long one template strand, DNA polymerase III can synthesize a complementary strand continuously by elongating the new DNA in the mandatory 5′ S 3′ directionDNA pol III remains in the replication fork on that template strand and continuously adds nucleotides to the new complementary strand as the fork progresses. The DNA strand made by this mechanism is called the leading strand.
33
lagging strand and okazaki fragments
DNA pol III must work along the other template strand in the direction away from the replication fork. The DNA strand elongating in this direction is called the lagging strand. In contrast to the leading strand, which elongates continuously, the lagging strand is synthesized discontinuously, as a series of segments. These segments of the lagging strand are called Okazaki fragments, after Reiji Okazaki, the Japanese scientist who discovered them. The fragments are about 1,000–2,000 nucleotides long in E. coli and 100–200 nucleotides long in eukaryotes.
34
dna ligase
. But DNA pol I cannot join the final nucleotide of this replacement DNA segment to the first DNA nucleotide of the adjacent Okazaki fragment. Another enzyme, DNA ligase, accomplishes this task, joining the sugar-phosphate backbones of all the Okazaki fragments into a continuous DNA strand (step
35
In eukaryotic cells, multiple copies of the complex, perhaps grouped into
Second, the DNA replication complex may not move along the DNA; rather, the DNA may move through the complex during the replication process. In eukaryotic cells, multiple copies of the complex, perhaps grouped into “factories,” may be anchored to the nuclear matrix, a framework of fibers extending through the interior of the nucleus. E
36
mismatch repair
Mismatched nucleotides sometimes evade proofreading by a DNA polymerase. In mismatch repair, other enzymes remove and replace incorrectly paired nucleotides that have resulted from replication errors.
37
nuclease and nucleotide excision repair
In many cases, a segment of the strand containing the damage is cut out (excised) by a DNAcutting enzyme—a nuclease—and the resulting gap is then filled in with nucleotides, using the undamaged strand as a template. The enzymes involved in filling the gap are a DNA polymerase and DNA ligase. One such DNA repair system is called nucleotide excision repair
38
r, a permanent change in the DNA | sequence is called a
mutation
39
In either case, mutations are the original | source of the variation
on which natural selection operates | during evolution and are ultimately responsible for the appearance of new species
40
For linear DNA, such as the DNA of eukaryotic chromosomes, | the usual replication machinery cannot c
complete the 5′ ends of daughter DNA strands. (This is another consequence of the fact that a DNA polymerase can add nucleotides only to the 3′ end of a preexisting polynucleotide.)
41
telomeres and how do we prevent the chromosome from being eroded away during rep?
But what protects the genes of linear eukaryotic chromosomes from being eroded away during successive rounds of DNA replication? Eukaryotic chromosomal DNA molecules have special nucleotide sequences called telomeres at their ends (Figure 16.21). Telomeres do not contain genes; instead, the DNA typically consists of multiple repetitions of one short nucleotide sequence. In each human telomere, for example, the six-nucleotide sequence TTAGGG is repeated between 100 and 1,000 times.
42
Telomeres have two protective functions.
First, specific proteins associated with telomeric DNA prevent the staggered ends of the daughter molecule from activating the cell’s systems for monitoring DNA damage. (Staggered ends of a DNA molecule, which often result from double-strand breaks, can trigger signal transduction pathways leading to cell cycle arrest or cell death.) Second, telomeric DNA acts as a kind of buffer zone that provides some protection against the organism’s genes shortening, somewhat like how the plastic-wrapped ends of a shoelace slow down its unraveling. Telomeres do not prevent the erosion of genes near the ends of chromosomes; they merely postpone it
43
what does telomerase do
An enzyme called telomerase catalyzes the lengthening of telomeres in eukaryotic germ cells, thus restoring their original length and compensating for the shortening that occurs during DNA replication. This enzyme contains its own RNA molecule that it uses as a template to artificially extend” the leading strand, allowing the lagging strand to maintain a given length. T
44
Normal shortening of telomeres may protect organisms | from cancer by l
limiting the number of divisions that somatic cells can undergo. Cells from large tumors often have unusually short telomeres, as we would expect for cells that have undergone many cell divisions. Further shortening would presumably lead to self-destruction of the tumor cells.
45
Telomerase activity is abnormally high in cancerous somatic | cells, suggesting that
its ability to stabilize telomere length | may allow these cancer cells to persist.
46
. Many cancer cells | do seem capable of u
unlimited cell division, as do immortal | strains of cultured cells
47
what have reserchers been studying for several years
For several years, researchers have studied inhibition of telomerase as a possible cancer therapy. While studies that inhibited telomerase in mice with tumors have led to the death of cancer cells, eventually the cells have restored the length of their telomeres by an alternative pathway. This is an area of ongoing research that may eventually yield useful cancer treatments.
48
histones
Proteins called histones are responsible for | the first level of DNA packing in chromatin
49
nucleosome
Each “bead” is a nucleosome, the basic unit of DNA packing; the “string” between beads is called linker DNA.
50
chromatin
Together, this complex of DNA and protein, called chromatin, fits into the nucleus through an elaborate, multilevel system of packing. Our current view of the successive levels of DNA packing in a chromosome is outlined in Figure 16.22. Study this figure carefully before reading further
51
30-nm fiber: The next level of packing results from
nteractions between the histone tails of one nucleosome and the linker DNA and nucleosomes on either side. The fifth type of histone is involved at this level.
52
how wide are looped domins and metaphase rep csomes
looped domains- 300 nm and meta- 1400 nm
53
describe interphase chromatin
Early on, biologists assumed that interphase chromatin was a tangled mass in the nucleus, like a bowl of spaghetti, but this is far from the case. Although an interphase chromosome lacks an obvious scaffold, its looped domains appear to be attached to the nuclear lamina, on the inside of the nuclear envelope, and perhaps also to fibers of the nuclear matrix. These attachments may help organize regions of chromatin where genes are active. The chromatin of each chromosome occupies a specific restricted area within the interphase nucleus, and the chromatin fibers of different chromosomes do not appear to be entangled
54
hetero and euchromatin
Even during interphase, the centromeres and telomeres of chromosomes, as well as other chromosomal regions in some cells, exist in a highly condensed state similar to that seen in a metaphase chromosome. This type of interphase chromatin, visible as irregular clumps with a light microscope, is called heterochromatin, to distinguish it from the less compacted, more dispersed euchromatin (“true chromatin”).
55
hetero v euchro - what can they each do and why
Because of its compaction, heterochromatic DNA is largely inaccessible to the machinery in the cell responsible for transcribing the genetic information coded in the DNA, a crucial early step in gene expression. In contrast, the looser packing of euchromatin makes its DNA accessible to this machinery, so the genes present in euchromatin can be transcribed. The chromosome is a dynamic structure that is condensed, loosened, modified, and remodeled as necessary for various cell processes, including mitosis, meiosis, and gene activity. Chemical modifications of histones affect the state of chromatin condensation and also have multiple effects on gene activity, as you’ll see in Concept 18.2