Inquiry into Life Twelfth Edition Chapter 25 Lecture PowerPoint to accompany Sylvia S. Mader...

Inquiry into LifeTwelfth Edition

Chapter 25

Lecture PowerPoint to accompany

Sylvia S. Mader

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

25.1 Control of Gene Expression

• Gene Expression in Bacteria

– Operon: A cluster of structural and regulatory genes

that acts as a unit.

• Sequences consists of:

– Promoter: A sequence of DNA where

transcription begins

– Operator: A sequence of DNA where a

repressor protein binds



– Example: The lac Operon in E. coli

• When lactose is absent:– The regulator gene codes for a repressor that is normally

active

– A repressor protein binds to the operator

– RNA polymerase cannot transcribe the three structural

genes of the operon (the structural genes are not

expressed)



– Example: The lac Operon in E. coli

• When lactose is present:– Lactose binds with the lac repressor

– Repressor is unable to bind to the operator

– Structural genes are transcribed

» Enzymes are produced

The lac Operon


• Gene Expression in Eukaryotes– “Housekeeping Genes”

• Not finely regulated• Products are always needed to some degree


• Gene Expression in Eukaryotes

– Levels of Gene Control• Chromatin Structure• Transcriptional Control• Posttranscriptional control• Translational control• Posttranslational control


• Levels of Gene Control

– Chromatin Structure• Chromatin packing is used to keep genes turned off• Heterochromatin: inactive genes located within darkly

staining portions of chromatin ex: Barr body• Euchromatin: loosely packed areas of active genes

– Euchromatin still needs processing before transcription occurs

– Chromatin remodeling complex pushes aside nucleosomes

X-inactivation



– Transcriptional Control• Most important level of control

• Enhancers and promoters on DNA are involved

– Transcription factors and activators are proteins which regulate

these sites

– Posttranscriptional Control• Removal of introns and splicing of exons

• Different patterns of splicing can occur



– Translational Control• Differences in the poly-A tails and/or guanine caps may

determine how long a mRNA is available for translation

• Specific hormones may also effect longevity of mRNA

– Posttranslational Control• Some proteins must be activated after synthesis

• Many proteins function only for a short time before they are

degraded or destroyed by the cell

Levels of Gene Control in Eukaryotes


• Transcription Factors and Activators– Transcription Factors- proteins which help RNA

polymerase bind to a promoter• Several transcription factors per gene form a transcription

initiation complex– Help in pulling DNA apart and in the release of RNA

polymerase for transcription

– Transcription Activators- proteins which speed up transcription

• Bind to an enhancer region on DNA• Enhancer and promoter may be far apart

– DNA forms a loop to bring them close together

Transcription Factors and Activators


• Signaling Between Cells– Cells are in constant communication– Cell produces a signaling molecule that binds to a

receptor on a target cell• Initiates a signal transduction pathway- series of

reactions that change the receiving cell’s behavior– May result in stimulation of a transcription

activator– Transcription activator will then turn on a gene

Signal Transduction Pathway

25.2 Cancer: A Failure of Genetic Control

• Contact Inhibition: When cells come into contact with neighboring cells, they stop dividing.

• Cancer cells lose contact inhibition and form tumors.• The tumor is deemed noncancerous or benign if it stays

as a single mass.• Cells are called cancerous when they invade

surrounding tissues.• Cancer cells can travel through the bloodstream and the

lymph and develop into secondary tumors.• Metastasis refers to cancer cells that have spread to

other parts of the body.

Development of Cancer


• Characteristics of Cancer Cells

– Cancer cells are genetically unstable.

– Cancer cells do not correctly regulate the cell cycle

– Cancer cells escape the signals for cell death.

– Cancer cells can survive and proliferate elsewhere in

the body.



– Cancer cells are genetically unstable.

• Multiple mutations, chromosome aberrations and may be

present.



– Cancer cells do not correctly regulate the cell cycle.

• Normal controls of the cell cycle do not work.

• The rate of cell division and the number of cells increase.



– Cancer cells escape the signals for cell death.

• Cancer cells do not respond to signals for apoptosis

– Telomeres of cancer cells do not shorten.



– Cancer cells can survive and proliferate elsewhere in

the body.

• As a tumor grows, it stimulates the formation of new blood

vessels to supply oxygen and nutrients to the cancerous

cells. This is called angiogenesis.


• Proto-oncogenes and Tumor Suppressor Genes

– Proto-oncogenes promote the cell cycle and prevent

apoptosis.

– Tumor suppressor genes inhibit the cell cycle and

promote apoptosis.


• Proto-oncogenes

– Mutate into cancer causing genes called oncogenes.

– An altered RAS protein is found in approximately 25%

of all tumors.

Activity of Ras Protein


• Tumor Suppressor Genes

– When these mutate, they no longer inhibit the cell

cycle.

– A gene called p53 normally prevents cell division if

there is damage to the DNA. If p53 mutates, the cells

may continue to divide indefinitely.

– About 1/2 of all human cancers have a mutation in

this gene.

Activity of p53 Tumor Suppressor


• Causes of Cancer

– Heredity

• Some types of cancer run in families

– Carcinogens

• Environmental agents that are mutagenic

• Radiation, some viruses, organic chemicals


• Diagnosis of Cancer

– Screening tests

• Pap smear, mammogram, colonoscopy

• Tumor marker tests

• Genetic tests

– Confirming diagnosis

• Biopsy, ultrasound, radioactive scans

Needle Biopsy of the Breast


• Treatment of Cancer

– Chemotherapy

– Radiation therapy

– Bone marrow transplant

– Future Treatments• Vaccines,

• Antiangiogenic drugs

Inquiry into Life Twelfth Edition Chapter 25 Lecture PowerPoint to accompany Sylvia S. Mader...

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