Chapter 16 Flashcards

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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
Q

single-strand binding proteins

A

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
Q

topoisomerase

A

Topoisomerase is an enzyme that
helps relieve this strain by breaking, swiveling, and rejoining
DNA strands.

27
Q

primer

A

. 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
Q

Primase starts a

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
Q

dna pols

A

Enzymes called DNA polymerases catalyze the synthesis

of new DNA by adding nucleotides to the 3′ end of a preexisting chain.

30
Q

The situation
in eukaryotes is more complicated, with at least 11 different
DNA polymerases discovered so far, although

A

the general

principles are the same.

31
Q

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

A

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
Q

leading strand

A

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
Q

lagging strand and okazaki fragments

A

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
Q

dna ligase

A

. 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
Q

In eukaryotic cells, multiple copies of the complex, perhaps grouped into

A

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
Q

mismatch repair

A

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
Q

nuclease and nucleotide excision repair

A

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
Q

r, a permanent change in the DNA

sequence is called a

A

mutation

39
Q

In either case, mutations are the original

source of the variation

A

on which natural selection operates

during evolution and are ultimately responsible for the appearance of new species

40
Q

For linear DNA, such as the DNA of eukaryotic chromosomes,

the usual replication machinery cannot c

A

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
Q

telomeres and how do we prevent the chromosome from being eroded away during rep?

A

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
Q

Telomeres have two protective functions.

A

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
Q

what does telomerase do

A

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
Q

Normal shortening of telomeres may protect organisms

from cancer by l

A

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
Q

Telomerase activity is abnormally high in cancerous somatic

cells, suggesting that

A

its ability to stabilize telomere length

may allow these cancer cells to persist.

46
Q

. Many cancer cells

do seem capable of u

A

unlimited cell division, as do immortal

strains of cultured cells

47
Q

what have reserchers been studying for several years

A

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
Q

histones

A

Proteins called histones are responsible for

the first level of DNA packing in chromatin

49
Q

nucleosome

A

Each “bead” is a nucleosome,
the basic unit of DNA packing; the “string”
between beads is called linker DNA.

50
Q

chromatin

A

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
Q

30-nm fiber: The next level of packing results from

A

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
Q

how wide are looped domins and metaphase rep csomes

A

looped domains- 300 nm and meta- 1400 nm

53
Q

describe interphase chromatin

A

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
Q

hetero and euchromatin

A

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
Q

hetero v euchro - what can they each do and why

A

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