Genetics: From Genes to Genomes, 5th edition
Genetics: From Genes to Genomes, 5th edition
5th Edition
ISBN: 9780073525310
Author: Leland H. Hartwell, Michael L. Goldberg, Janice A. Fischer, Leroy Hood, Charles F. Aquadro
Publisher: McGraw-Hill Education
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Chapter 16, Problem 14P
Summary Introduction

a.

To determine:

Whether the target genes with enhancers containing binding sites for Myc-Max encode proteins and Mad-Max encode proteins would arrest the cell cycle or drive the cell cycle forward along with an explanation.

Introduction:

Myc is a transcription factor which controls the process of cell proliferation. The mutation in the Myc gene contributes to many cases of cancer. The Myc protein contains a leucine zipper dimerization domain and a specialized DNA binding domain.

Summary Introduction

b.

To draw:

A diagram that shows the control region for a target gene, proteins binding to the enhancer and the process of transcription.

Introduction:

The Max and Mad proteins help in resolving the problem of cancer. Like Myc, the Max and Mad contain a specialized DNA binding domain and a leucine zipper. They do not homodimerize readily and do not bind DNA with high affinity.

Summary Introduction

c.

To determine:

The ways by which myc, max and mad proteins regulate cell proliferation.

Introduction:

The Myc-Max and Mad-Max form heterodimers readily and bind with the DNA domain. They bind at the same sites on the enhancers of the same target genes. Myc contains an activation domain, and Mad contains a repressor domain.

Summary Introduction

d.

To determine:

Whether the cancer-causing mutations in Myc is loss-of-function or gain-of-function mutation.

Introduction:

The Max gene is expressed in all the cell at all times. The Mad gene is expressed in resting cells, whereas the Myc gene starts to express when cells are about to divide. Mad and Myc proteins are unstable with respect to the Max protein.

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Chapter 16 Solutions

Genetics: From Genes to Genomes, 5th edition

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