Genetics: A Conceptual Approach © 2009 W. H. Freeman and Company Benjamin A. Pierce Genetics: A Conceptual Approach THIRD EDITION CHAPTER 17 Control of Gene Expression in Eukaryotes © 2009 W. H. Freeman and Company Copyright 2008 © W. H. Freeman and Company

Anopheles mosquitoes transmit Plasmodium falciparum, one of the protozoan parasites that causes malaria, to humans. The parasite survives in humans by altering the expression of its surface proteins through gene regulation, thereby evading the human immune defenses. [Dr. Dennis Kunkel/Visuals Unlimited.]

Figure 17. 1 Plasmodium falciparum infects human red blood cells Figure 17.1 Plasmodium falciparum infects human red blood cells. A cross section through an infected human red blood cell, showing single-celled malaria parasites (green). [Omikron/Photo Researchers.]

Figure 17.2 The acetylation of histone proteins alters chromatin structure and permits some transcription factors to bind to DNA.

Figure 17.2 The acetylation of histone proteins alters chromatin structure and permits some transcription factors to bind to DNA.

Figure 17.3 Flowering in Arabidopsis is controlled in part by FLD, a gene that encodes a deacetylase enzyme. This enzyme removes acetyl groups from histone proteins in chromatin surrounding FLC, a gene that suppresses flowering. The removal of the acetyl groups from the histones restores chromatin structure and represses the transcription of FLC, thereby allowing the plant to flower.

Figure 17.3 Flowering in Arabidopsis is controlled in part by FLD, a gene that encodes a deacetylase enzyme. This enzyme removes acetyl groups from histone proteins in chromatin surrounding FLC, a gene that suppresses flowering. The removal of the acetyl groups from the histones restores chromatin structure and represses the transcription of FLC, thereby allowing the plant to flower.

Figure 17.3 (part 1) Flowering in Arabidopsis is controlled in part by FLD, a gene that encodes a deacetylase enzyme. This enzyme removes acetyl groups from histone proteins in chromatin surrounding FLC, a gene that suppresses flowering. The removal of the acetyl groups from the histones restores chromatin structure and represses the transcription of FLC, thereby allowing the plant to flower.

Figure 17.3 (part 1) Flowering in Arabidopsis is controlled in part by FLD, a gene that encodes a deacetylase enzyme. This enzyme removes acetyl groups from histone proteins in chromatin surrounding FLC, a gene that suppresses flowering. The removal of the acetyl groups from the histones restores chromatin structure and represses the transcription of FLC, thereby allowing the plant to flower.

Figure 17.3 (part 2) Flowering in Arabidopsis is controlled in part by FLD, a gene that encodes a deacetylase enzyme. This enzyme removes acetyl groups from histone proteins in chromatin surrounding FLC, a gene that suppresses flowering. The removal of the acetyl groups from the histones restores chromatin structure and represses the transcription of FLC, thereby allowing the plant to flower.

Figure 17.3 (part 2) Flowering in Arabidopsis is controlled in part by FLD, a gene that encodes a deacetylase enzyme. This enzyme removes acetyl groups from histone proteins in chromatin surrounding FLC, a gene that suppresses flowering. The removal of the acetyl groups from the histones restores chromatin structure and represses the transcription of FLC, thereby allowing the plant to flower.

Figure 17.4 Transcriptional activator proteins bind to sites on DNA and stimulate transcription. Most act by stimulating or stabilizing the assembly of the basal transcription apparatus.

Figure 17.4 Transcriptional activator proteins bind to sites on DNA and stimulate transcription. Most act by stimulating or stabilizing the assembly of the basal transcription apparatus.

Figure 17.5 The consensus sequences in the promoters of three eukaryotic genes illustrate the principle that different sequences can be mixed and matched in different combinations. A different transcriptional activator protein binds to each consensus sequence, and so each promoter responds to a unique combination of activator proteins.

Figure 17.6 Transcription is activated by GAL4 in response to galactose. GAL4 binds to the UASG site and controls the transcription of genes in galactose metabolism.

Figure 17.6 Transcription is activated by GAL4 in response to galactose. GAL4 binds to the UASG site and controls the transcription of genes in galactose metabolism.

Figure 17.7 An insulator blocks the action of an enhancer on a promoter when the insulator lies between the enhancer and the promoter.

Figure 17.7 An insulator blocks the action of an enhancer on a promoter when the insulator lies between the enhancer and the promoter.

Figure 17.8 Multiple response elements (MREs) are found in the upstream region of the metallothionein gene. The basal transcription apparatus binds near the TATA box. In response to heavy metals, activator proteins bind to several MREs and stimulate transcription. The TRE response element is the binding site for transcription factor AP1, which is stimulated by phorbol esters. In response to glucocorticoid hormones, steroid-receptor proteins bind to the GRE response element located approximately 250 nucleotides upstream of the metallothionein gene and stimulate transcription.

Figure 17.8 Multiple response elements (MREs) are found in the upstream region of the metallothionein gene. The basal transcription apparatus binds near the TATA box. In response to heavy metals, activator proteins bind to several MREs and stimulate transcription. The TRE response element is the binding site for transcription factor AP1, which is stimulated by phorbol esters. In response to glucocorticoid hormones, steroid-receptor proteins bind to the GRE response element located approximately 250 nucleotides upstream of the metallothionein gene and stimulate transcription.

Figure 17.9 Alternative splicing leads to the production of the small t antigen and the large T antigen in the mammalian virus SV40.

Figure 17.9 Alternative splicing leads to the production of the small t antigen and the large T antigen in the mammalian virus SV40.

Figure 17.10 Alternative splicing controls sex determination in Drosophila.

Figure 17.10 Alternative splicing controls sex determination in Drosophila.

Figure 17.10 (part 1) Alternative splicing controls sex determination in Drosophila.

Figure 17.10 (part 1) Alternative splicing controls sex determination in Drosophila.

Figure 17.10 (part 2) Alternative splicing controls sex determination in Drosophila.

Figure 17.10 (part 2) Alternative splicing controls sex determination in Drosophila.

Figure 17. 11 Alternative splicing of tra pre-mRNA Figure 17.11 Alternative splicing of tra pre-mRNA. Two alternative 3′ splice sites are present.

Figure 17. 11 Alternative splicing of tra pre-mRNA Figure 17.11 Alternative splicing of tra pre-mRNA. Two alternative 3′ splice sites are present.

Figure 17. 11 (part 1) Alternative splicing of tra pre-mRNA Figure 17.11 (part 1) Alternative splicing of tra pre-mRNA. Two alternative 3′ splice sites are present.

Figure 17. 11 (part 1) Alternative splicing of tra pre-mRNA Figure 17.11 (part 1) Alternative splicing of tra pre-mRNA. Two alternative 3′ splice sites are present.

Figure 17. 11 (part 2) Alternative splicing of tra pre-mRNA Figure 17.11 (part 2) Alternative splicing of tra pre-mRNA. Two alternative 3′ splice sites are present.

Figure 17. 11 (part 2) Alternative splicing of tra pre-mRNA Figure 17.11 (part 2) Alternative splicing of tra pre-mRNA. Two alternative 3′ splice sites are present.

Figure 17.12a RNA silencing leads to the degradation of mRNA, or the inhibition of translation or transcription. Small interfering RNAs (siRNAs) degrade mRNA by cleavage.

Figure 17.12a RNA silencing leads to the degradation of mRNA, or the inhibition of translation or transcription. Small interfering RNAs (siRNAs) degrade mRNA by cleavage.

Figure 17.12b RNA silencing leads to the degradation of mRNA, or the inhibition of translation or transcription. MicroRNAs (miRNAs) lead to the inhibition of translation.

Figure 17.12b RNA silencing leads to the degradation of mRNA, or the inhibition of translation or transcription. MicroRNAs (miRNAs) lead to the inhibition of translation.

Figure 17.12c RNA silencing leads to the degradation of mRNA, or the inhibition of translation or transcription. Some siRNAs methylate histone proteins or DNA, inhibiting transcription.

Figure 17.12c RNA silencing leads to the degradation of mRNA, or the inhibition of translation or transcription. Some siRNAs methylate histone proteins or DNA, inhibiting transcription.

Figure 17.13 The expression of some eukaryotic genes is regulated by the availability of components required for translation. In this example, exposure to an antigen stimulates an increased availability of initiation factors and a subsequent increase in protein synthesis, leading to T-cell proliferation.

Figure 17.13 The expression of some eukaryotic genes is regulated by the availability of components required for translation. In this example, exposure to an antigen stimulates an increased availability of initiation factors and a subsequent increase in protein synthesis, leading to T-cell proliferation.

Figure 17.13 (part 1) The expression of some eukaryotic genes is regulated by the availability of components required for translation. In this example, exposure to an antigen stimulates an increased availability of initiation factors and a subsequent increase in protein synthesis, leading to T-cell proliferation.

Figure 17.13 (part 1) The expression of some eukaryotic genes is regulated by the availability of components required for translation. In this example, exposure to an antigen stimulates an increased availability of initiation factors and a subsequent increase in protein synthesis, leading to T-cell proliferation.

Figure 17.13 (part 2) The expression of some eukaryotic genes is regulated by the availability of components required for translation. In this example, exposure to an antigen stimulates an increased availability of initiation factors and a subsequent increase in protein synthesis, leading to T-cell proliferation.

Figure 17.13 (part 2) The expression of some eukaryotic genes is regulated by the availability of components required for translation. In this example, exposure to an antigen stimulates an increased availability of initiation factors and a subsequent increase in protein synthesis, leading to T-cell proliferation.

Figure 17.14 Arabidopsis thaliana is a model genetic organism that serves as an important subject for research on genetic processes in plants. [Photograph courtesy of Anand P. Tyagi and Luca Comai, Dept. of Biology, University of Washington, Seattle.]

Figure 17.14 (part 1) Arabidopsis thaliana is a model genetic organism that serves as an important subject for research on genetic processes in plants.

Figure 17.14 (part 2) Arabidopsis thaliana is a model genetic organism that serves as an important subject for research on genetic processes in plants.

Figure 17.14 (part 3) Arabidopsis thaliana is a model genetic organism that serves as an important subject for research on genetic processes in plants. [Photograph courtesy of Anand P. Tyagi and Luca Comai, Dept. of Biology, University of Washington, Seattle.]

Figure 17.14 (part 4) Arabidopsis thaliana is a model genetic organism that serves as an important subject for research on genetic processes in plants.

Figure 17.14 (part 5) Arabidopsis thaliana is a model genetic organism that serves as an important subject for research on genetic processes in plants.