lecture 2

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1. Compare the organization of prokaryotic and eukaryotic genomes.

Prokaryotic

 Usually circular

 Smaller

 Found in the

nucleoid region

 Less elaborately

structured and folded

Eukaryotic

 Complexed with a large

amount of protein to form chromatin

 Highly extended and

tangled during interphase

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2. Describe the current model for progressive levels of DNA packing.

 Nucleosome  basic unit of DNA packing [formed from DNA wound around a protein core that consists of 2

copies each of the 4 types of histone (H2A, H2B, H3, H4)]  A 5th histone (H1) attaches near the bead when the

chromatin undergoes the next level of packing

 30 nm chromatin fiber  next level of packing; coil with 6 nucleosomes per turn

 the 30 nm chromatin forms looped domains, which are attached to a nonhistone protein scaffold (contains 20,000 – 100,000 base pairs)

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3. Explain how histones influence folding in eukaryotic DNA.



Histones



small proteins rich in

basic amino acids that bind to DNA,

forming chromatin



Contain a high proportion of positively

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4. Distinguish between heterochromatin and euchromatin.

Heterochromatin

 Chromatin that

remains highly

condensed during interphase and is NOT actively

transcribed

Euchromatin

 Chromatin that is

less condensed

during interphase and IS actively transcribed

 Becomes highly

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5. Describe where satellite DNA is found and what role it may play in the cell.

 Satellite DNA  highly repetitive DNA

consisting of short unusual nucleotide sequences that are tandemly repeated 1000’s of times

 It is found at the tips of chromosomes and

the centromere

 Its function is not known, perhaps it plays a

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6. Describe the role of telomeres in solving the end-replication problem with the lagging DNA strand.

 Telomere  series of short tandem

repeats at the ends of eukaryotic

chromosomes; prevents chromosomes from shortening with each replication cycle

 Telomerase  enzyme that periodically

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7. Using the genes for rRNA as an example, explain how multigene families of identical genes can be advantageous for a cell.

 Multigene family  a collection of genes

that are similar or identical in sequence and presumably of common ancestral origin

 Include genes for the major rRNA

molecules, huge tandem repeats of these genes enable cells to make millions of

ribosomes during active protein synthesis

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8. Using _{-globin and}_{-globin genes as examples,}

describe how multigene families of nonidentical genes probably evolve, including the role of

transposition.

 They arise over time from mutations that

accumulate in duplicated genes

 Can be clustered on the same chromosome

or scattered throughout the genome

 Original α & β genes evolved from

duplication of a common ancestral globin gene

 Transposition separated the α globin and β

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9. Explain gene amplification.

 Gene amplification  the selective

replication of certain genes that is a

potent way of increasing expression of the rRNA genes, enabling more ribosomes to be made

 Selective gene loss  in certain tissues,

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10. Describe the effects of transposons and retrotransposons.

 Transposons  jump and interrupt the normal

functioning may increase or decrease production of one or more proteins

- can carry a gene that can be activated when

inserted downstream from an active promoter and vice versa

 Retrotransposons  transposable elements that

move within a genome by means of an RNA

intermediate, a transcript of the retrotransposon DNA

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11. Explain immunoglobin genes.

 Immunoglobin genes  genes that encode

antibodies

 Basic immunoglobin molecule  consists of

four polypeptide chains held by disulfide bridges

- each chain has 2 regions: constant and variable

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12. Explain the chromatin modifications of DNA methylation, genomic imprinting, and histone acetylation.

 DNA methylation  the attachment of methyl groups

(-CH₃) to DNA bases

-Inactive DNA is usually highly methylated (adding methyl groups inactivates DNA)

 Genomic imprinting  where methylation permanently

turns off either the maternal or paternal allele of certain genes at the start of development

 Histone acetylation  the attachment of acetyl groups

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13. Explain the potential role that promoters and enhancers play in transcriptional control.

Promoters

 Include the proximal

control elements

 Produces a low rate of

initiation with few RNA transcripts

 Unless  DNA

sequences can improve the efficiency by

binding additional transcription factors

Enhancers

 The more distant

control elements

 Bending of the DNA

enables the

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14. Compare the arrangement of coordinately controlled genes in prokaryotes and

eukaryotes.

Prokaryotic

 Prokaryotic genes that

are turned on and off together are often

clustered into operons which are transcribed into one mRNA

molecule and

translated together

Eukaryotic

 Eukaryotic genes

coding for enzymes of a metabolic

pathway are often scattered over

different

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15. Explain how eukaryotic genes can be

coordinately expressed and give some examples of coordinate gene expression in eukaryotes.

 Associated with specific regulatory DNA

sequences or enhancers that are recognized by a single type of transcription factor that activates or represses a group of genes in synchrony

- heat shock response  series of proteins that

help stabilize and repair

- Steroid hormone action  steroids activate

protein receptors which activate genes

- Cellular differentiation  the genes produce

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16. Explain why the ability to rapidly degrade mRNA can be an adaptive advantage for

prokaryotes.



Prokaryotic mRNA molecules are

degraded by enzymes after only a

few minutes



thus bacteria can

quickly alter patterns of protein

synthesis in response to

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17. Describe the importance of mRNA

degradation in eukaryotes, describe how it can be prevented.



The longevity of a mRNA affects how

much protein synthesis it directs;

those that are viable longer can

produce more of their protein



Control mechanisms of gene

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18. Explain how gene expression may be

controlled at translation and post-translation.

 Translational  binding of translation repressor protein to the 5’ end of a particular mRNA can prevent ribosome attachment

- translation of all mRNAs can be blocked by the inactivation of certain initiation factors

 Posttranslational  last level

- many eukaryotic polypeptides must be modified or transported before becoming biologically active by adding phosphates, chemical groups, etc.

- selective degradation of particular proteins and regulation of enzyme activity are also control

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19. Describe the normal control mechanisms that limit cell growth and division.



Proto-oncogenes



gene that

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20. Briefly describe the four mechanisms that can convert proto-oncogenes to

oncogenes.

1. Movement of DNA within the genome 

chromosomes have been broken and rejoined

2. Gene amplification  sometimes more copies of

oncogenes are present in a cell than is normal

3. Point mutation  a slight change in the

nucleotide sequence might produce a growth-stimulating protein that is more active or more resistant to degradation than the normal protein

4. Changes in tumor-suppressor genes that

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21. Explain how changes in tumor-suppressor genes can be involved in transforming normal cells into cancerous cells.

 Frequency of

mutation is close to 50% for the p53

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22. Explain how oncogenes are involved in virus-induced cancers.

