review Some questions.
1. A common fallacious argument against evolution is it is impossible for a random
process to increase complexity. This is bunk. Explain why natural selection is NOT
random. Explain why natural selection can increase complexity, causing a simple
replicator RNA to evolve over many generations into a primitive genome of linked
catalytic RNAs.
2. The very first self replicating molecules were probably terriblelow rate, and terrible
fidelity. Why would that increase the rate at which evolution would occur?
3. Explain why selection favors the formation of primitive cellsthat is, explain the
reproductive advantage of cellularity. In a primitive proto-cell, is there any advantage to
having the different genes on a single RNA, or is it just as good to have them as
separate pieces of RNA?
4. A common fallacious argument against evolution is genomes are so perfectly put
together, with all the genes working with each other; it is impossible for a random
process to produce such a perfect system. This is bunk. Why do we not see lots of
inefficient organismsis it that no inefficient organisms are made, or does something
else happen?
5. Some populations of Escherichia coli have become pathogens, and no longer ever find
themselves in an environment with lactose. Describe the series of events that, over
evolutionary time, will cause these populations to lose the lac genes. How does selection
drive simplification? Is this "progress?" Is there a single definition of "progress?" Is this
process efficient, or is it slow and wasteful? Would an individual cell decide that the
lac genes were no longer useful, and get rid of them, enhancing the fitness of its
descendants?
6. Most Escherichia coli live in an environment in which lactose is frequently the only
source of carbon. Describe how selection is a conservative force in this environment,
ensuring that the lac genes are maintained without functionally significant changes.
What sort of evolutionary change can happen to the lactose utilization genes under these
circumstances?
7. Mutation is random. Are most mutations beneficial, neutral, or deleterious? Why is
most of the work done by natural selection conservative, aimed at eliminating changes to
the genome?
8. A large duplication in the genome might seem to be a neutral mutationafter all, its
not adding anything new or different. However, this is generally a deleterious mutation,
negatively affecting the fitness of the genome. Why? Under what circumstances could a
duplication be a beneficial mutation?
9. How do duplications open up new possibilities for evolution? What other types of
mutations can increase the diversity of genes within a genome?
10. How can a gene that is necessary for a cells function (and thus under selection
pressure) evolve?
11. Imagine a culture of bacterial cells. Divide the culture in half, then grow each half
under absolutely identical conditions for 10,000 generations. Would the two cultures
have identical genomes at the end of this process? Why or why not? Would they have
identical phenotypes (characteristics) at the end of this process? Why or why not?
12. Do the same thought experiment, but now the two cultures grown are under different
conditionssay, 28 and pH 6 versus 37 and pH 7. Would the two cultures have
identical genomes at the end of this process? Why or why not? Would they have
identical phenotypes (characteristics) at the end of this process? Why or why not?
13. Selection is a conservative force in a constant environment. Is it a conservative force
in a fragmented and varying environment?
14. What is meant by consensus for DNA binding proteins? The regulatory protein
CAP binds to the genome of E. coli in approximately 300 places. How would you
determine the consensus binding site for CAP? Would you expect it to be the same as the
consensus binding site for RNA polymerase?
15. Why is most regulation of gene expression done by regulating transcription
initiation? Is there any advantage to regulating later steps in gene expression?
16. What are the essential characteristics of a protein that negatively regulates
transcription of a gene? Would you expect such a protein to be produced constitutively
or not? At a high level or a low level?
17. Researchers have a good knowledge of the consensus binding site for CAP, and so
we can examine a DNA sequence and determine where in that sequence CAP will bind.
Ditto for RNA polymerase. Does this allow us to determine which genes are positively
regulated by CAP, and which negatively regulated by CAP, or is it impossible to tell this
from looking at DNA sequences?
18. What is the essential feature of a protein that positively regulates transcription that
distinguishes it from a negative regulator? Can such a protein also act as a negative
regulator? What determines where a protein binds to the genome?
19. The lys operon is responsible for the production of the amino acid lysine. What
characteristics would you expect in a positive regulator of transcription that would result
in feedback regulation of the lys operon? What characteristics would you expect for a
negative regulator of transcription that would result in feedback regulation of the lys
operon?
20. The lys operon has 5 genes, lysA through lysE. What sequences would you design to
make the lys operon expressed only in the presence of lactose? Only in the presence of
lactose and absence of tryptophan? Only in the presence of lactose AND glucose and the
absence of tryptophan?
21. The lys operon, as noted, has 5 genes. How many promoters? How many start
codons? How many stop codons? How many mRNAs are produced?
22. Nostoc is a type of bacterium that lives in diverse environments, and can grow
photoautotrophically or respire aerobically or anaerobically or ferment. Mycoplasma is a
type of bacterium that lives as a parasite inside our cells. Which would you expect to
have the larger genome? Which would have more genes for regulatory proteins? Why?
23. Would you expect the DNA that encodes a riboswitch to be upstream or downstream
of a promoter? Upstream or downstream of the gene that it regulates? Repression of
transcription is easy enoughjust block RNA polymerase. What can a riboswitch block
or cover up to prevent translation?
24. Why is it thought that regulation by riboswitch is more ancient than regulation using
repressors and activators of transcription?