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BIOLOGY Campbell • Reece • Urry • Cain • Wasserman • Minorsky • Jackson © 2015 Pearson Education Ltd TENTH EDITION Global Edition Lecture Presentation by Nicole Tunbridge and Kathleen Fitzpatrick 16 Nucleic Acids and Inheritance

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BIOLOGY

Campbell • Reece • Urry • Cain • Wasserman • Minorsky • Jackson

© 2015 Pearson Education Ltd

TENTH EDITION

Global Edition

Lecture Presentation by

Nicole Tunbridge and

Kathleen Fitzpatrick

16Nucleic Acids and

Inheritance

© 2015 Pearson Education Ltd

Life’s Operating Instructions

a) In 1953, James Watson and Francis Crick introduced

an elegant double-helical model for the structure of

deoxyribonucleic acid, or DNA

b) Hereditary information is encoded in DNA and

reproduced in all cells of the body

c) This DNA program directs the development of

biochemical, anatomical, physiological, and

(to some extent) behavioral traits

© 2015 Pearson Education Ltd

Figure 16.1

© 2015 Pearson Education Ltd

Figure 16.1a

© 2015 Pearson Education Ltd

a) DNA is copied during DNA replication, and cells can

repair their DNA

© 2015 Pearson Education Ltd

Concept 16.1: DNA is the genetic material

a) Early in the 20th century, the identification of the

molecules of inheritance loomed as a major challenge

to biologists

© 2015 Pearson Education Ltd

The Search for the Genetic Material: Scientific Inquiry

a) When T. H. Morgan’s group showed that genes are

located on chromosomes, the two components of

chromosomes—DNA and protein—became

candidates for the genetic material

b) The role of DNA in heredity was first discovered

by studying bacteria and the viruses that

infect them

© 2015 Pearson Education Ltd

Evidence That DNA Can Transform Bacteria

a) The discovery of the genetic role of DNA began with

research by Frederick Griffith in 1928

b) Griffith worked with two strains of a bacterium, one

pathogenic and one harmless

© 2015 Pearson Education Ltd

a) When he mixed heat-killed remains of the pathogenic

strain with living cells of the harmless strain, some

living cells became pathogenic

b) He called this phenomenon transformation, now

defined as a change in genotype and phenotype due

to assimilation of foreign DNA

© 2015 Pearson Education Ltd

Figure 16.2

Living S cells(pathogeniccontrol)

Experiment

Results

Living R cells(nonpathogeniccontrol)

Heat-killed S cells(nonpathogeniccontrol)

Mouse dies Mouse healthy Mouse healthy Mouse dies

Mixture of heat-killed S cells andliving R cells

Living S cells

© 2015 Pearson Education Ltd

a) In 1944, Oswald Avery, Maclyn McCarty, and Colin

MacLeod announced that the transforming substance

was DNA

b) Many biologists remained skeptical, mainly because

little was known about DNA

© 2015 Pearson Education Ltd

Evidence That Viral DNA Can Program Cells

a) More evidence for DNA as the genetic material came

from studies of viruses that infect bacteria

b) Such viruses, called bacteriophages (or phages),

are widely used in molecular genetics research

c) A virus is DNA (sometimes RNA) enclosed by a

protective coat, often simply protein

© 2015 Pearson Education Ltd

Figure 16.3

Phage

head

DNA

Tail

sheath

Tail fiber

Genetic

material

Bacterial

cell

100 n

m

© 2015 Pearson Education Ltd

Animation: Phage T2 Reproductive Cycle

© 2015 Pearson Education Ltd

a) In 1952, Alfred Hershey and Martha Chase showed

that DNA is the genetic material of a phage known as

T2

b) They designed an experiment showing that only one

of the two components of T2 (DNA or protein) enters

an E. coli cell during infection

c) They concluded that the injected DNA of the phage

provides the genetic information

© 2015 Pearson Education Ltd

Figure 16.4

Experiment

Batch 1: Radioactive sulfur (35S) in phage protein

Batch 2: Radioactive phosphorus (32P) in phage DNA

Labeled phagesinfect cells.

Agitation frees outsidephage parts from cells.

Centrifuged cellsform a pellet.

Radioactivity(phage protein)found in liquid

Pellet

Centrifuge

Radioactiveprotein

RadioactiveDNA

Radioactivity (phageDNA) found in pellet

Centrifuge

Pellet

1 2

4

3

4

© 2015 Pearson Education Ltd

Figure 16.4a

Experiment

Batch 1: Radioactive sulfur (35S) in phage protein

Labeled phagesinfect cells.

Agitation frees outside phage parts from cells.

Centrifuged cellsform a pellet.

Radioactivity(phage protein)found in liquid

Radioactiveprotein

Pellet

Centrifuge

1 2 3

4

© 2015 Pearson Education Ltd

Figure 16.4b

Pellet

Centrifuge

Batch 2: Radioactive phosphorus (32P) in phage DNA

RadioactiveDNA

Radioactivity (phage DNA) found in pellet

Labeled phagesinfect cells.

Agitation frees outside phage parts from cells.

Centrifuged cellsform a pellet.

Experiment

1 2 3

4

© 2015 Pearson Education Ltd

Animation: Hershey-Chase Experiment

© 2015 Pearson Education Ltd

Additional Evidence That DNA Is the Genetic Material

a) It was known that DNA is a polymer of nucleotides,

each consisting of a nitrogenous base, a sugar, and a

phosphate group

b) In 1950, Erwin Chargaff reported that DNA

composition varies from one species to the next

c) This evidence of diversity made DNA a more credible

candidate for the genetic material

© 2015 Pearson Education Ltd

Figure 16.5

5′ end

Thymine (T)

Adenine (A)

Cytosine (C)

Guanine (G)

Nitrogenous

bases

Sugar–

phosphate

backbone

3′ end

Nitrogenous

base

Sugar

(deoxyribose)DNA

nucleotide

Phosphate

© 2015 Pearson Education Ltd

Animation: DNA and RNA Structure

© 2015 Pearson Education Ltd

a) Two findings became known as Chargaff’s rules

a)The base composition of DNA varies between species

b)In any species the number of A and T bases are equal

and the number of G and C bases are equal

b) The basis for these rules was not understood until the

discovery of the double helix

© 2015 Pearson Education Ltd

Building a Structural Model of DNA: Scientific Inquiry

a) After DNA was accepted as the genetic material, the

challenge was to determine how its structure

accounts for its role in heredity

b) Maurice Wilkins and Rosalind Franklin were using a

technique called X-ray crystallography to study

molecular structure

c) Franklin produced a picture of the DNA molecule

using this technique

© 2015 Pearson Education Ltd

Figure 16.6

(a) Rosalind Franklin (b) Franklin’s X-ray diffraction

photograph of DNA

© 2015 Pearson Education Ltd

Figure 16.6a

(a) Rosalind Franklin

© 2015 Pearson Education Ltd

Figure 16.6b

(b) Franklin’s X-ray diffraction

photograph of DNA

© 2015 Pearson Education Ltd

a) Franklin’s X-ray crystallographic images of DNA

enabled Watson to deduce that DNA was helical

b) The X-ray images also enabled Watson to deduce the

width of the helix and the spacing of the nitrogenous

bases

c) The pattern in the photo suggested that the DNA

molecule was made up of two strands, forming a

double helix

© 2015 Pearson Education Ltd

Figure 16.7

(a) Key features of

DNA structure

(b) Partial chemical structure

0.34 nm

3′ end

5′ endT

T

T

A

A

A

C

C

C

G

G

G

AT1 nm

TA

C G

CG

AT3.4 nm

CG

CG

C G

C G

3′ end

5′ end

Hydrogen bond

T A

G C

A T

C G

(c) Space-filling

model

© 2015 Pearson Education Ltd

Figure 16.7a

(a) Key features of DNA structure

0.34 nm

1 nm

3.4 nm

T

T

T

A

A

A

C

C

C

G

G

G

AT

TA

C G

CG

AT

CG

CG

C G

C G

© 2015 Pearson Education Ltd

Figure 16.7b

(b) Partial chemical structure

3′ end

5′ end

3′ end

5′ end

Hydrogen bond

T A

G C

A T

C G

© 2015 Pearson Education Ltd

Figure 16.7c

(c) Space-filling model

© 2015 Pearson Education Ltd

Animation: DNA Double Helix

© 2015 Pearson Education Ltd

Video: Stick Model of DNA (Deoxyribonucleic Acid)

© 2015 Pearson Education Ltd

Video: Surface Model of DNA (Deoxyribonucleic Acid)

© 2015 Pearson Education Ltd

a) Watson and Crick built models of a double helix to

conform to the X-rays and chemistry of DNA

b) Franklin had concluded that there were two outer

sugar-phosphate backbones, with the nitrogenous

bases paired in the molecule’s interior

c) Watson built a model in which the backbones were

antiparallel (their subunits run in opposite directions)

© 2015 Pearson Education Ltd

a) At first, Watson and Crick thought the bases paired

like with like (A with A, and so on), but such pairings

did not result in a uniform width

b) Instead, pairing a purine with a pyrimidine resulted in

a uniform width consistent with the X-ray data

© 2015 Pearson Education Ltd

Figure 16.UN02

Purine + purine: too wide

Pyrimidine + pyrimidine: too narrow

Purine + pyrimidine: width

consistent with X-ray data

© 2015 Pearson Education Ltd

a) Watson and Crick reasoned that the pairing was more

specific, dictated by the base structures

b) They determined that adenine (A) paired only with

thymine (T), and guanine (G) paired only with

cytosine (C)

c) The Watson-Crick model explains Chargaff’s rules: in

any organism the amount of A = T, and the amount of

G = C

© 2015 Pearson Education Ltd

Figure 16.8

Sugar

Sugar

Adenine (A)

Sugar

Sugar

Thymine (T)

Cytosine (C)Guanine (G)

© 2015 Pearson Education Ltd

Concept 16.2: Many proteins work together in DNA replication and repair

a) The relationship between structure and function is

manifest in the double helix

b) Watson and Crick noted that the specific base pairing

suggested a possible copying mechanism for genetic

material

© 2015 Pearson Education Ltd

The Basic Principle: Base Pairing to a Template Strand

a) Since the two strands of DNA are complementary,

each strand acts as a template for building a new

strand in replication

b) In DNA replication, the parent molecule unwinds, and

two new daughter strands are built based on base-

pairing rules

© 2015 Pearson Education Ltd

Figure 16.9-1

(a) Parental

molecule

A

A

A

T

T

T

G

G C

C

© 2015 Pearson Education Ltd

Figure 16.9-2

(a) Parental

molecule(b) Separation of parental

strands into templates

A

A

A

T

T

T

G

G C

C

A

A

A

T

T

T

G

G C

C

© 2015 Pearson Education Ltd

Figure 16.9-3

(a) Parental

molecule(b) Separation of parental

strands into templates

A

A

A

T

T

T

G

G C

C

A

A

A

T

T

T

G

G C

C

A

A

A

T

T

T

G

G C

C

A

A

A

T

T

T

G

G C

C

(c) Formation of new strands

complementary to template

strands

© 2015 Pearson Education Ltd

a) Watson and Crick’s semiconservative model of

replication predicts that when a double helix

replicates, each daughter molecule will have one old

strand (derived or “conserved” from the parent

molecule) and one newly made strand

b) Competing models were the conservative model (the

two parent strands rejoin) and the dispersive model

(each strand is a mix of old and new)

© 2015 Pearson Education Ltd

Figure 16.10

(a) Conservative

model

(b) Semiconserva-

tive model

(c) Dispersive

model

Parent cell

First

replication

Second

replication

© 2015 Pearson Education Ltd

a) Experiments by Matthew Meselson and Franklin Stahl

supported the semiconservative model

b) They labeled the nucleotides of the old strands with a

heavy isotope of nitrogen, while any new nucleotides

were labeled with a lighter isotope

© 2015 Pearson Education Ltd

a) The first replication produced a band of hybrid DNA,

eliminating the conservative model

b) A second replication produced both light and hybrid

DNA, eliminating the dispersive model and supporting

the semiconservative model

© 2015 Pearson Education Ltd

Figure 16.11

Bacteria cultured

in medium with 15N

(heavy isotope)

Experiment

Results

Conclusion

Bacteria transferred

to medium with 14N

(lighter isotope)

DNA sample

centrifuged

after first

replication

DNA sample

centrifuged

after second

replication

Less dense

More dense

Predictions: First replication Second replication

Conservative

model

Semiconservative

model

Dispersive

model

1 2

43

© 2015 Pearson Education Ltd

Figure 16.11a

Bacteria cultured

in medium with 15N

(heavy isotope)

Experiment

Results

Bacteria transferred

to medium with 14N

(lighter isotope)

DNA samplecentrifugedafter firstreplication

DNA samplecentrifugedafter secondreplication

Less dense

More dense

1 2

3 4

© 2015 Pearson Education Ltd

Figure 16.11b

Conclusion

Predictions: First replication Second replication

Conservative

model

Semiconservative

model

Dispersive

model

© 2015 Pearson Education Ltd

DNA Replication: A Closer Look

a) The copying of DNA is remarkable in its speed and

accuracy

b) More than a dozen enzymes and other proteins

participate in DNA replication

© 2015 Pearson Education Ltd

Getting Started

a) Replication begins at particular sites called origins of

replication, where the two DNA strands are

separated, opening up a replication “bubble”

b) A eukaryotic chromosome may have hundreds or

even thousands of origins of replication

c) Replication proceeds in both directions from each

origin, until the entire molecule is copied

© 2015 Pearson Education Ltd

Figure 16.12

Origin of

replication

0.5

µm

0.2

5 µ

m

Bacterial

chromosome

Two daughter

DNA molecules

Replication

bubble

Parental (template)

strandDaughter

(new) strand

Replication

fork

Double-

stranded

DNA molecule

(a) Origin of replication in an E. coli cell (b) Origins of replication in a eukaryotic cell

Origin of

replication Eukaryotic chromosome

Double-stranded

DNA molecule

Parental (template)

strandDaughter (new)

strand

Replication

forkBubble

Two daughter DNA molecules

© 2015 Pearson Education Ltd

Figure 16.12a

0.5

µm

Origin of

replication

Bacterial

chromosome

Two daughter

DNA molecules

Replication

bubble

Parental (template) strand

Daughter

(new) strand

Replication

forkDouble-stranded

DNA molecule

(a) Origin of replication in an E. coli cell

© 2015 Pearson Education Ltd

Figure 16.12aa

0.5

µm

© 2015 Pearson Education Ltd

Figure 16.12b

0.2

5 µ

m

(b) Origins of replication in a eukaryotic cell

Origin of replication Eukaryotic chromosome

Double-stranded

DNA molecule

Parental (template) strand

Daughter (new)

strand

Replication

forkBubble

Two daughter DNA molecules

© 2015 Pearson Education Ltd

Figure 16.12ba

0.2

5 µ

m

© 2015 Pearson Education Ltd

Animation: Origins of Replication

© 2015 Pearson Education Ltd

a) At the end of each replication bubble is a replication

fork, a Y-shaped region where

new DNA strands are elongating

b)Helicases are enzymes that untwist the double helix

at the replication forks

c) Single-strand binding proteins bind to and stabilize

single-stranded DNA

d)Topoisomerase corrects “overwinding” ahead of

replication forks by breaking, swiveling, and rejoining

DNA strands

© 2015 Pearson Education Ltd

Figure 16.13

Topoisomerase

Primase

RNA

primer

Replication

fork

5′

3′

5′

5′

3′

Helicase

Single-strand binding

proteins

3′

© 2015 Pearson Education Ltd

a) DNA polymerases cannot initiate synthesis of a

polynucleotide; they can only add nucleotides to an

existing 3′ end

b) The initial nucleotide strand is a short RNA primer

© 2015 Pearson Education Ltd

a) An enzyme called primase can start an RNA chain

from scratch and adds RNA nucleotides one at a time

using the parental DNA as a template

b) The primer is short (5–10 nucleotides long), and the

3′ end serves as the starting point for the new DNA

strand

© 2015 Pearson Education Ltd

Synthesizing a New DNA Strand

a) Enzymes called DNA polymerases catalyze the

elongation of new DNA at a replication fork

b) Most DNA polymerases require a primer and a DNA

template strand

c) The rate of elongation is about 500 nucleotides per

second in bacteria and 50 per second in human cells

© 2015 Pearson Education Ltd

a) Each nucleotide that is added to a growing DNA

strand is a nucleoside triphosphate

b) dATP supplies adenine to DNA and is similar to the

ATP of energy metabolism

c) The difference is in their sugars: dATP has

deoxyribose while ATP has ribose

d) As each monomer of dATP joins the DNA strand, it

loses two phosphate groups as a molecule of

pyrophosphate

© 2015 Pearson Education Ltd

Figure 16.14

5′ 5′3′

3′

5′ 5′

New strand Template strand

Sugar

Phosphate Base

OH

A T

C

C

G

G

A

C

Nucleotide

DNApoly-

merase

OH

Pyro-phosphate

2 P i

P iP

3′

3′

A T

C

C

G

G

A

C

T

© 2015 Pearson Education Ltd

Antiparallel Elongation

a) The antiparallel structure of the double helix affects

replication

b) DNA polymerases add nucleotides only to the free 3′

end of a growing strand; therefore, a new DNA strand

can elongate only in the 5′ to 3′ direction

© 2015 Pearson Education Ltd

Figure 16.15

Leading strand Lagging strand

Leading strand

Parental DNA

Lagging strand

Primer

Overview

Origin of replication

Overall

directions

of replication Origin of replication

RNA primer

Sliding clamp

DNA pol III

Continuous

elongation in the

5′ to 3′ direction

5′

5′

5′

5′

5′

5′

3′ 3′

3′3′

3′

3′

DNA pol III starts to

synthesize leading

strand.

1

2

© 2015 Pearson Education Ltd

Figure 16.15a

Leading strand Lagging strand

Leading strandLagging strand

Primer

Overview

Origin of replication

Overall directions

of replication

© 2015 Pearson Education Ltd

Figure 16.15b

Parental DNA

Origin of replication

RNA primer

Sliding clamp

DNA pol III

5′

5′

5′

3′ 3′

3′

DNA pol III starts to

synthesize leading

strand.

1

5′

3′

5′

3′

5′

3′

2 Continuous

elongation in the

5′ to 3′ direction

© 2015 Pearson Education Ltd

Animation: Leading Strand

© 2015 Pearson Education Ltd

a) Along one template strand of DNA, the DNA

polymerase synthesizes a leading strand

continuously, moving toward the replication fork

© 2015 Pearson Education Ltd

a) To elongate the other new strand, called the lagging

strand, DNA polymerase must work in the direction

away from the replication fork

b) The lagging strand is synthesized as a series of

segments called Okazaki fragments, which are

joined together by DNA ligase

© 2015 Pearson Education Ltd

Figure 16.16Overview

12

1

1

2

1

2

1

1

2

5′

3′

3′

5′5′3′

3′

3′ 3′5′

5′5′

5′3′

3′

5′3′

5′3′

5′3′

5′3′

5′3′

5′3′

1

2 5

6

4

3

Origin of replication

Lagging

strand

Leading

strand

Lagging

strand

Leading

strandOverall directions

of replication

RNA primer

for fragment 2

Okazaki

fragment 2DNA pol III

makes Okazaki

fragment 2.

DNA pol I

replaces RNA

with DNA.

DNA ligase

forms bonds

between DNA

fragments.

Overall direction of replication

Okazaki

fragment 1

DNA pol III

detaches.

RNA primer

for fragment 1

Template

strand

DNA pol III

makes Okazaki

fragment 1.

Origin of

replication

Primase makes

RNA primer.

5′

© 2015 Pearson Education Ltd

Figure 16.16a

12

Overview

Origin of replication

Lagging

strand

Leading

strand

Lagging

strand

Leading

strandOverall directions

of replication

© 2015 Pearson Education Ltd

Figure 16.16b-1

5′

3′

5′5′3′

3′Template

strand

Origin of

replication

Primase makes

RNA primer.

1

© 2015 Pearson Education Ltd

Figure 16.16b-2

5′

3′

5′5′3′

3′Template

strand

Origin of

replication

Primase makes

RNA primer.

1

5′3′

5′

3′

5′3′

RNA primer

for fragment 1

DNA pol III

makes Okazaki

fragment 1.

1

2

© 2015 Pearson Education Ltd

Figure 16.16b-3

5′

3′

5′5′3′

3′Template

strand

Origin of

replication

Primase makes

RNA primer.

1

5′3′

5′

3′

5′3′

RNA primer

for fragment 1

DNA pol III

makes Okazaki

fragment 1.

1

2

1

3

3′

3′5′

5′

Okazaki

fragment 1

DNA pol III

detaches.

© 2015 Pearson Education Ltd

DNA pol III

makes Okazaki

fragment 2.

Figure 16.16c-1

2

5′

3′

5′3′

4

RNA primer

for fragment 2Okazaki

fragment 2

1

© 2015 Pearson Education Ltd

Figure 16.16c-2

DNA pol III

makes Okazaki

fragment 2.2

5′

3′

5′3′

4

RNA primer

for fragment 2Okazaki

fragment 2

1

5′3′

DNA pol I

replaces RNA

with DNA.

5′3′

1

2

5

© 2015 Pearson Education Ltd

Figure 16.16c-3

DNA ligaseforms bondsbetween DNAfragments.

Overall direction of replication

DNA pol III

makes Okazaki

fragment 2.2

5′

3′

5′3′

4

RNA primer

for fragment 2Okazaki

fragment 2

1

5′3′

DNA pol I

replaces RNA

with DNA.

5′3′

1

2

5

6

5′3′

5′3′

1

2

© 2015 Pearson Education Ltd

Animation: Lagging Strand

© 2015 Pearson Education Ltd

Figure 16.17

Overview

5′

3′

Lagging

strand

Leading

strand

Leading

strand

Lagging

strandLeading strand

Leading strand

template

Origin of

replication

Overall directions

of replication

5′

3′

5′3′

5′

5′

3′

3′3′

Single-strand

binding proteins

Helicase

Parental

DNA

DNA pol III

Primer

Primase

Lagging

strand

Lagging strand

template

DNA pol III

DNA pol I5′

DNA ligase

123

4

5

© 2015 Pearson Education Ltd

Figure 16.17a

Overview

Lagging

strand

Leading

strand

Leading

strand

Lagging

strand

Origin of

replication

Overall directions

of replication

© 2015 Pearson Education Ltd

Figure 16.17b

5′

5′

3′

3′3′

Single-strand

binding proteins

Helicase

Parental

DNA

DNA pol III

Primer

Primase

Leading

strand

Leading strand

template

5

© 2015 Pearson Education Ltd

Figure 16.17c

4

3 2 1

5′

5′3′

5′

3′

Lagging

strand

DNA pol III

DNA pol I DNA ligase

Lagging strand

template

© 2015 Pearson Education Ltd

Animation: DNA Replication Overview

© 2015 Pearson Education Ltd

Animation: DNA Replication Review

© 2015 Pearson Education Ltd

Table 16.1

© 2015 Pearson Education Ltd

Table 16.1a

© 2015 Pearson Education Ltd

Table 16.1b

© 2015 Pearson Education Ltd

The DNA Replication Complex

a) The proteins that participate in DNA replication form a

large complex, a “DNA replication machine”

b) The DNA replication machine may be stationary

during the replication process

c) Recent studies support a model in which DNA

polymerase molecules “reel in” parental DNA and

“extrude” newly made daughter DNA molecules

© 2015 Pearson Education Ltd

Figure 16.18

Leading strand template

5′

5′

5′

5′3′

3′

3′

3′

3′ 3′

5′

5′

Leading strand

Lagging strand

Lagging

strand

template

DNA pol III

Connecting proteinHelicase

Parental DNA

DNA pol III

© 2015 Pearson Education Ltd

BioFlix: DNA Replication

© 2015 Pearson Education Ltd

Proofreading and Repairing DNA

a) DNA polymerases proofread newly made DNA,

replacing any incorrect nucleotides

b) In mismatch repair of DNA, repair enzymes correct

errors in base pairing

c) DNA can be damaged by exposure to harmful

chemical or physical agents such as cigarette smoke

and X-rays; it can also undergo spontaneous

changes

d) In nucleotide excision repair, a nuclease cuts out

and replaces damaged stretches of DNA

© 2015 Pearson Education Ltd

Figure 16.19-1

Nuclease

5′

5′

5′

5′

3′

3′

3′

3′

© 2015 Pearson Education Ltd

Figure 16.19-2

Nuclease

5′

5′

5′

5′

3′

3′

3′

3′

5′

5′

3′

3′

DNA

polymerase

© 2015 Pearson Education Ltd

Figure 16.19-3

Nuclease

5′

5′

5′

5′

3′

3′

3′

3′

5′

5′

3′

3′

DNA

polymerase

DNA

ligase

5′

3′5′

3′

© 2015 Pearson Education Ltd

Evolutionary Significance of Altered DNA Nucleotides

a) Error rate after proofreading repair is low but

not zero

b) Sequence changes may become permanent and can

be passed on to the next generation

c) These changes (mutations) are the source of the

genetic variation upon which natural selection

operates

© 2015 Pearson Education Ltd

Replicating the Ends of DNA Molecules

a) Limitations of DNA polymerase create problems for

the linear DNA of eukaryotic chromosomes

b) The usual replication machinery provides no way to

complete the 5′ ends, so repeated rounds of

replication produce shorter DNA molecules with

uneven ends

c) This is not a problem for prokaryotes, most of which

have circular chromosomes

© 2015 Pearson Education Ltd

Figure 16.20

Ends of parental

DNA strands

Lagging strand

Parental strand

RNA primer

Last fragmentNext-to-last

fragment

Lagging strand

Leading strand

Removal of primers and

replacement with DNA

where a 3′ end is available

3′

5′

5′

Second round

of replication

Further rounds

of replication

New lagging strand

New leading strand

Shorter and shorter daughter molecules

5′

3′

3′

5′

3′

5′

3′

© 2015 Pearson Education Ltd

Figure 16.20a

Ends of parental

DNA strands

Lagging strand

Parental strand

RNA primer

Last fragment

Next-to-last

fragment

Lagging strand

Leading strand

Removal of primers and

replacement with DNA

where a 3′ end is available

3′

5′

5′

3′

5′

3′

© 2015 Pearson Education Ltd

Figure 16.20b

5′

Second round

of replication

Further rounds

of replication

New lagging strand

New leading strand

Shorter and shorter daughter molecules

5′

3′

3′

5′

3′

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a) Eukaryotic chromosomal DNA molecules have

special nucleotide sequences at their ends called

telomeres

b) Telomeres do not prevent the shortening of DNA

molecules, but they do postpone the erosion of genes

near the ends of DNA molecules

c) It has been proposed that the shortening of telomeres

is connected to aging

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Figure 16.21

1 µm

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a) If chromosomes of germ cells became shorter in

every cell cycle, essential genes would eventually be

missing from the gametes they produce

b) An enzyme called telomerase catalyzes the

lengthening of telomeres in germ cells

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a) The shortening of telomeres might protect cells from

cancerous growth by limiting the number of cell

divisions

b) There is evidence of telomerase activity in cancer

cells, which may allow cancer cells to persist

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Concept 16.3: A chromosome consists of a DNA molecule packed together with proteins

a) The bacterial chromosome is a double-stranded,

circular DNA molecule associated with a small

amount of protein

b) Eukaryotic chromosomes have linear DNA molecules

associated with a large amount

of protein

c) In a bacterium, the DNA is “supercoiled” and found in

a region of the cell called the nucleoid

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a) In the eukaryotic cell, DNA is precisely combined with

proteins in a complex called chromatin

b) Chromosomes fit into the nucleus through an

elaborate, multilevel system of packing

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Figure 16.22

DNA, the

double helixHistones Nucleosomes,

or “beads on

a string”

(10-nm fiber)

30-nm fiberLooped

domains

(300-nm fiber)

Metaphase

chromosome

DNA

double helix

(2 nm in diameter)

Nucleosome

(10 nm in diameter)30-nm fiber

Loops Scaffold

HistonesHistone tail

H1

300-nm

fiber

Chromatid

(700 nm)

Replicated

chromosome

(1,400 nm)

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Figure 16.22a

DNA, the

double helix

Histones Nucleosomes, or “beads on

a string” (10-nm fiber)

DNA

double helix

(2 nm in diameter)

Nucleosome

(10 nm in diameter)

HistonesHistone tail

H1

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Figure 16.22aa

DNA double helix

(2 nm in diameter)

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Figure 16.22ab

Nucleosome

(10 nm in diameter)

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Figure 16.22b

30-nm fiber

Looped domains

(300-nm fiber)

Metaphase

chromosome

30-nm fiber

Loops Scaffold

300-nm fiber

Chromatid

(700 nm)

Replicated

chromosome

(1,400 nm)

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Figure 16.22ba

30-nm fiber

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Figure 16.22bb

Loops Scaffold

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Figure 16.22bc

Chromatid

(700 nm)

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Animation: DNA Packing

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Video: Cartoon and Stick Model of a NucleosomalParticle

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a) Chromatin undergoes changes in packing during the

cell cycle

b) At interphase, some chromatin is organized into a 10-

nm fiber, but much is compacted into a 30-nm fiber,

through folding and looping

c) Interphase chromosomes occupy specific restricted

regions in the nucleus and the fibers of different

chromosomes do not become entangled

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Figure 16.23

5 µm

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Figure 16.23a

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Figure 16.23b

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Figure 16.23c

5 µm

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a) Most chromatin is loosely packed in the nucleus

during interphase and condenses prior to mitosis

b) Loosely packed chromatin is called euchromatin

c) During interphase a few regions of chromatin

(centromeres and telomeres) are highly condensed

into heterochromatin

d) Dense packing of the heterochromatin makes it

difficult for the cell to express genetic information

coded in these regions

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a) Histones can undergo chemical modifications that

result in changes in chromatin organization

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Figure 16.UN01

Base Percentage

Source of DNA Adenine Guanine Cytosine Thymine

Sea urchin 32.8 17.7 17.3 32.1

Salmon 29.7 20.8 20.4 29.1

Wheat 28.1 21.8 22.7

E. coli 24.7 26.0

Human 30.4 30.1

Ox 29.0

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Figure 16.UN02

Purine + purine: too wide

Pyrimidine + pyrimidine: too narrow

Purine + pyrimidine: width

consistent with X-ray data

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Figure 16.UN03

Sugar-phosphate

backbone

Nitrogenous

bases

Hydrogen bond

G

G

G

G

G

C

C

C

C

C

A T

T A

A T

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Figure 16.UN04

DNA pol III synthesizes

leading strand continuously

Parental

DNA

Helicase

Primase synthesizes

a short RNA primer

3′

5′

DNA pol I replaces the RNA

primer with DNA nucleotides

3′

5′

3′

5′

DNA pol III starts DNA

synthesis at 3′ end of primer,

continues in 5′ → 3′ direction

Lagging strand synthesized

in short Okazaki fragments,

later joined by DNA ligase

Origin of

replication

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Figure 16.UN05

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Figure 16.UN06