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Cell division Chapter 10 Genes and Development

Cell division Chapter 10 Genes and Development. Fig. 10.1-1 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display

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Cell division

Chapter 10Genes and Development

Fig. 10.1-1

Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Bacterial cell

Bacterial chromosome:Double-stranded DNA

Origin ofreplication

Fig. 10.1Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Bacterial cell

Septum

Bacterial chromosome:Double-stranded DNA

Origin ofreplication

Fig. 10.2

Fig. 10.3a

Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Septum

FtsZ protein

Chromosome

Prokaryotes

No nucleus, usuallyhave single circularchromosome. After DNA is replicated, it ispartitioned in the cell.After cell elongation,FtsZ protein assemblesinto a ring and facilitatesseptation and celldivision.

Fig. 10.3

Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Septum

FtsZ protein

Chromosome

ChromosomeMicrotubule

Nucleus

Kinetochore microtubule

Centrioles Kinetochore

Polar microtubule

Spindle pole body

Kinetochore microtubule

Centriole

Prokaryotes Some Protists Other Protists Animals

Kinetochore microtubule

Polar microtubule

No nucleus, usually have single circularchromosome. After DNA is replicated, it ispartitioned in the cell.After cell elongation,FtsZ protein assemblesinto a ring and facilitatesseptation and celldivision.

Nucleus present andnuclear enveloperemains intact duringcell division.Chromosomes line up.Microtubule fibers passthrough tunnels in thenuclear membrane andset up an axis forseparation ofreplicatedchromosomes, and celldivision.

A spindle of micro-tubules forms betweentwo pairs of centrioles atopposite ends of thecell. The spindle passes through one tunnel inthe intact nuclearenvelope. Kinetochoremicrotubules formbetween kinetochoreson the chromosomesand the spindle polesand pull the chromo-somes to each pole.

Nuclear enveloperemains intact; spindlemicrotubules form insidethe nucleus betweenspindle pole bodies. Asingle kinetochoremicrotubule attaches toeach chromosome andpulls each to a pole.

Spindle microtubulesbegin to form betweencentrioles outside ofnucleus. Centrioles moveto the poles and thenuclear envelope breaksdown. Kinetochoremicrotubules attachkinetochores ofchromosomes to spindlepoles. Polar microtubulesextend toward the centerof the cell and overlap.

Yeasts

Central spindleof microtubules

Fragmentsof nuclearenvelope

Table 10.1

Fig. 10.5-1

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Chromosome

Fig. 10.5-2

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Chromosome Rosettes of Chromatin Loops

Scaffold protein

Fig. 10.5-3

Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Chromosome Rosettes of Chromatin Loops Chromatin Loop

Chromatin loop

Scaffold protein Scaffoldprotein

Fig. 10.5-4

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Chromosome Rosettes of Chromatin Loops Chromatin Loop Solenoid

Chromatin loop

Scaffold protein Scaffoldprotein

Fig. 10.5

Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Chromosome Rosettes of Chromatin Loops Chromatin Loop Solenoid

Nucleosome

Histone core

Chromatin loop

Scaffold protein Scaffoldprotein

DNA

DNA Double Helix (duplex)

Animation of DNA coiling

DNA coiling and cells dividing

Fig. 10.6

Fig. 10.7

Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Homologous chromosomes Homologous chromosomes

Sister chromatids

Sister chromatids

Centromere

Replication

Kinetochore

Kinetochores

Cohesin proteinsCentromere

Fig. 10.8

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G1

G2

S Interphase

MitosisM Phase

Cytokinesis

M Phase

G2

S G1

Metaphase

Prophase

Anaphase

Telophase

Prometaphase

Cell cycle

Fig. 10.9

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Chromatid

Kinetochore

Cohesinproteins

Centromereregion ofchromosome

Metaphasechromosome

Kinetochoremicrotubules

Fig. 10.10

Red = CohesinGreen = KinetochoreBlue = Chromosome

Fig. 10.11aCopyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

© Andrew S. Bajer, University of Oregon

INTERPHASE G2

Nucleus

Nucleolus

Aster

80 µmCentrioles(replicated;animalcells only)

Nuclearmembrane

• DN A has been replicated• Centrioles replicate (animal cells)• Cell prepares for division

Chromatin(replicated)

Fig. 10.11bCopyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Prophase

80 µm

• Chromosomes condense and become visible• Chromosomes appear as two sister chromatids held together at the centromere• Cytoskeleton is disassembled: spindle begins to form• Golgi and ER are dispersed• Nuclear envelope breaks down

Mitotic spindlebeginning to form

Condensedchromosomes

© Andrew S. Bajer, University of Oregon

MITOSIS

Prometaphase

80 µm

• Chromosomes attach to microtubules at the kinetochores• Each chromosome is oriented such that the kinetochores of sister chromatids are attached to microtubules from opposite poles.• Chromosomes move to equator of the cell

Centromere andkinetochore

Mitoticspindle

Fig. 10.11c Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

© Andrew S. Bajer, University of Oregon

MITOSIS

Metaphase

• All chromosomes are aligned at equator of the cell, called the metaphase plate• Chromosomes are attached to opposite poles and are under tension

Polar microtubule

80 µmChromosomesaligned on

metaphase plateKinetochoremicrotubule

Fig. 10.11dCopyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

© Andrew S. Bajer, University of Oregon

MITOSIS

Fig. 10.12Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Centrioles

Sister chromatids

Aster

57 µm

Kinetochoremicrotubule

Metaphaseplate

Polarmicrotubule

© Andrew S. Bajer, University of Oregon

Anaphase

Chromosomes

• Proteins holding centromeres of sister chromatids are degraded, freeing individual chromosomes• Chromosomes are pulled to opposite poles (anaphase A)• Spindle poles move apart (anaphase B)

Kinetochoremicrotubule

80 µmPolar

microtubule

Fig. 10.11eCopyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

© Andrew S. Bajer, University of Oregon

MITOSIS

Fig. 10.13 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Metaphase

Pole Pole

Pole Pole 2 µm

Overlappingmicrotubules

Late Anaphase

Overlappingmicrotubules

© Dr. Jeremy Pickett-Heaps

Telophase

Polar microtubule

Nucleus reforming

• Chromosomes are clustered at opposite poles and decondense• Nuclear envelopes re-form around chromosomes• Golgi complex and ER re-form

80 µm

Kinetochoremicrotubule

Fig. 10.11f Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

© Andrew S. Bajer, University of Oregon

MITOSIS

Fig. 10.11g Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Cleavage furrow

CYTOKINESIS

• In animal cells, cleavage furrow forms to divide the cells• In plant cells, cell plate forms to divide the cells

80 µm

© Andrew S. Bajer, University of Oregon

Fig. 10.11

Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

INTERPHASE G2

Prophase Prometaphase Metaphase Anaphase Telophase

Nucleus

Nucleolus

Aster

Chromosomes

Polar microtubule

Nucleus reforming

Cleavage furrow

80 µm80 µm80 µm

CYTOKINESISMITOSIS

Centrioles(replicated;animalcells only)

Nuclearmembrane

• DN A has been replicated• Centrioles replicate (animal cells)• Cell prepares for division

• Chromosomes condense and become visible• Chromosomes appear as two sister chromatids held together at the centromere• Cytoskeleton is disassembled: spindle begins to form• Golgi and ER are dispersed• Nuclear envelope breaks down

• Chromosomes attach to microtubules at the kinetochores• Each chromosome is oriented such that the kinetochores of sister chromatids are attached to microtubules from opposite poles.• Chromosomes move to equator of the cell

• All chromosomes are aligned at equator of the cell, called the metaphase plate• Chromosomes are attached to opposite poles and are under tension

• Proteins holding centromeres of sister chromatids are degraded, freeing individual chromosomes• Chromosomes are pulled to opposite poles (anaphase A)• Spindle poles move apart (anaphase B)

• Chromosomes are clustered at opposite poles and decondense• Nuclear envelopes re-form around chromosomes• Golgi complex and ER re-form

• In animal cells, cleavage furrow forms to divide the cells• In plant cells, cell plate forms to divide the cells

Polar microtubule

Kinetochoremicrotubule

Chromatin(replicated)

80 µm 80 µm 80 µm80 µm

Mitotic spindlebeginning to form

Condensedchromosomes

Centromere andkinetochore

Mitoticspindle

Chromosomesaligned on

metaphase plateKinetochoremicrotubule

Polarmicrotubule

Kinetochoremicrotubule

© Andrew S. Bajer, University of Oregon

Fig. 10.14

Fig. 10.15Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Cell wall

Nucleus

0.7 µm

Vesicles containingmembrane componentsfusing to form cell plate

© B.A. Palevits & E.H. Newcomb/BPS/Tom Stack & AssociatesPlants

Fig. 10.16-1

Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

SCIENTIFIC THINKING

Hypothesis: There are positive regulators of mitosis.

Fig. 10.16-2

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SCIENTIFIC THINKING

Hypothesis: There are positive regulators of mitosis.

Prediction: Frog oocytes are arrested in G2 of meiosis I. They canbe induced to mature (undergo meiosis) by progesteronetreatment. If maturing oocytes contain a positive regulator of celldivision, injection of cytoplasm should induce an immatureoocyte to undergo meiosis.

Fig. 10.16-4Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Removecytoplasm

Arrested oocyte Oocyte in meiosis I

SCIENTIFIC THINKING

Hypothesis: There are positive regulators of mitosis.

Prediction: Frog oocytes are arrested in G2 of meiosis I. They canbe induced to mature (undergo meiosis) by progesteronetreatment. If maturing oocytes contain a positive regulator of celldivision, injection of cytoplasm should induce an immatureoocyte to undergo meiosis.

Test: Oocytes are induced with progesterone, then cytoplasmfrom these maturing cells is injected into immature oocytes.

Result: Injected oocytes progress G2 from into meiosis I.

Injectcytoplasm

Progesterone-treated oocyte

Fig. 10.16-5Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Removecytoplasm

Arrested oocyte Oocyte in meiosis I

SCIENTIFIC THINKING

Hypothesis: There are positive regulators of mitosis.

Prediction: Frog oocytes are arrested in G2 of meiosis I. They canbe induced to mature (undergo meiosis) by progesteronetreatment. If maturing oocytes contain a positive regulator of celldivision, injection of cytoplasm should induce an immatureoocyte to undergo meiosis.

Test: Oocytes are induced with progesterone, then cytoplasmfrom these maturing cells is injected into immature oocytes.

Result: Injected oocytes progress G2 from into meiosis I.

Conclusion: The progesterone treatment causes production of apositive regulator of maturation: Maturation Promoting Factor (MPF).

Injectcytoplasm

Progesterone-treated oocyte

Fig. 10.16-7 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Removecytoplasm

Arrested oocyte Oocyte in meiosis I

M phase cell G1 phase cell Fused cells

SCIENTIFIC THINKING

Hypothesis: There are positive regulators of mitosis.

Prediction: Frog oocytes are arrested in G2 of meiosis I. They canbe induced to mature (undergo meiosis) by progesteronetreatment. If maturing oocytes contain a positive regulator of celldivision, injection of cytoplasm should induce an immatureoocyte to undergo meiosis.

Test: Oocytes are induced with progesterone, then cytoplasmfrom these maturing cells is injected into immature oocytes.

Result: Injected oocytes progress G2 from into meiosis I.

Conclusion: The progesterone treatment causes production of apositive regulator of maturation: Maturation Promoting Factor (MPF).

Prediction: If mitosis is driven by positive regulators, thencytoplasm from a mitotic cell should cause a G1 cell to entermitosis.

Test: M phase cells are fused with G1 phase cells, then thenucleus from the G1 phase cell is monitored microscopically.

Conclusion: Cytoplasm from M phase cells contains a positiveregulator that causes a cell to enter mitosis.

Injectcytoplasm

Progesterone-treated oocyte

Fig. 10.17

Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

G1 S G2 MG2 M G1 S G2 M

Co

nc

entr

ati

on

Low

HighMPF activityCyclin

Fig. 10.18

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G2

M

S G1

Spindle checkpointG2/M checkpoint

G1/S checkpoint(Start or restriction point)

Fig. 10.19

Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Cyclin

P

Cyclin-dependent kinase(Cdk)

P

Fig. 10.20Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

• Growth factors

• Size of cell

G2

M

SG1

Spindle Checkpoint

APCCdc2/Mitotic Cyclin

• Chromosomes attached at metaphase plate

• Replication completed• DNA integrity

G2/M Checkpoint

G1/S Checkpoint

Cdk1/Cyclin B

• Nutritional state of cell

Yeast

Fig. 10.21Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

• Growth factors

• Size of cell

G2

M

SG1

Spindle Checkpoint

APCCdk1/Cyclin B

• Chromosomes attached at metaphase plate

• Replication completed• DNA integrity

G2/M Checkpoint

G1/S Checkpoint

Cdc2/G1Cyclin

• Nutritional state of cell

Animals

Fig. 10.22 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Nucleus

Chromosome

RAF

MEK

ERK

E2F

E2F

Rb

Rb

P

P P

P P

PP

P

P

P

Growth factor

Cyclins/proteinsfor S phase

Cyclins/proteinsfor S phase

RAF

MEK

ERK

Nucleus

Rb

Rb

E2F

Chromosome

P

PRASRAS

MAP kinase pathway Rb

Fig. 10.23-1

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1. DNA damage is caused by heat, radiation, or chemicals.

2. Cell division stops, and p53 triggers enzymes to repair damaged region.

3. p53 triggers the destruction of cells damaged beyond repair.

p53 allows cells withrepaired DNA to divide.

DNA repair enzyme

p53protein

No

rma

l p

53

Fig. 10.23

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1. DNA damage is caused by heat, radiation, or chemicals.

2. Cell division stops, and p53 triggers enzymes to repair damaged region.

3. p53 triggers the destruction of cells damaged beyond repair.

p53 allows cells withrepaired DNA to divide.

1. DNA damage is caused by heat, radiation, or chemicals.

2. The p53 protein fails to stop cell division and repair DNA. Cell divides without repair to damaged DNA.

3. Damaged cells continue to divide. If other damage accumulates, the cell can turn cancerous.

DNA repair enzyme

Cancer cell

p53protein

No

rma

l p

53

A

bn

orm

al

p5

3

Abnormalp53 protein

Fig. 10.24

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Proto-oncogenes

Growth factor receptor: more per cell in many breast cancers.

Ras protein: activated by mutations in 20–30% of all cancers.

Src kinase: activated by mutations in 2–5% of all cancers.

Tumor-suppressor Genes

Rb protein: mutated in 40% of all cancers.

p53 protein: mutated in 50% of all cancers.

Cell cyclecheckpoints

Rasprotein

Rbprotein p53

protein

Srckinase