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BIOL 151L – Study Questions – Chapter 12 – The Cell Cycle – pp. 228-245
(Prepare for class for Monday, October 5, 2009)
1. Be sure to read the Overview introduction to this chapter. To what central tenet of biology does the
phrase "Omnis cellula e cellula" refer (i.e. what does this mean)?
2. One obvious function of cell division is to allow a single-celled organism to divide to form duplicate
offspring. What various functions does cell division serve in a multicellular organism? What happens in a
multicellular organism if cell division gets out of control?
3. There are terms (and new vocabulary words) in this chapter that you must learn. Be sure you learn and
understand the meaning of the following: genome, somatic cells versus gametes, chromatin, sister
chromatids, centromere, mitosis, prophase, metaphase, anaphase, telophase, meiosis, cell cycle,
interphase (and G1 phase, S phase, and G2 phase), mitotic spindle (what is this made of?), cytokinesis (and
cleavage furrow and cell plate), restriction point and G0 phase, checkpoint, protein kinases and cyclins,
transformation, and metastasis.
4. What is the cell cycle? Understand how mitosis fits into the cell cycle in relation to interphase. Also,
study the four stages of mitosis (prophase, metaphase, anaphase, and telophase) and learn what happens at
each phase. Make a list for yourself of what happens during each phase (study pages 232-233). What
happens during cytokinesis?
**5. Make a simple drawing of the mitotic spindle at metaphase, showing the connections between the
fibers of the spindle and the chromosomes. Be sure to draw the chromosomes as doubled, with two sister
chromatids held together by the centromere. How will these sister chromatids separate during anaphase
of mitosis?
6. What kind of a chromosome does a prokaryotic (bacterial) cell have? Explain the process by which
bacteria divide and produce two new cells. How is this related to mitosis evolutionarily?
7. How can the cell-cycle control system be compared to the control device of an automatic washing
machine? What is a checkpoint, and what checks must a cell pass before it "decides" to pass one of these
restriction points? What is the significance of the G1 checkpoint and the G0 phase?
8. What two important classes of regulatory proteins within the cell act to control the sequential events of
the cell cycle? What is MPF, and what is its significance as a trigger? What internal signal acts at the M
phase checkpoint? What external signals, both chemical and physical, can influence cell division?
9. How is cancer related to the cell cycle and the various controls that regulate it? What are some ways in
which cells of a malignant tumor are abnormal?
BIOL 151L – Study Questions – Chapter 13 – Meiosis and Sexual Life Cycles – pp. 248-261
(Prepare for class for Wednesday, October 7, 2009)
*** Be sure to read the introduction to this unit on Genetics, an interview with Terry Orr-Weaver (pp.
246-247), who studies the process of meiosis, and what can go wrong, in Drosophila, the fruit fly.
1. What is the difference between asexual and sexual reproduction? To which is the term "clone"
applicable? Which generates more genetic variation in the offspring? What is the relationship between a
gene, a locus, and a genome?
2. How many chromosomes are found in a human somatic cell? How many pairs of homologous
chromosomes are there? What does the term "homologous" mean? Where do the two chromosomes in a
homologous pair come from? How many pair(s) of sex chromosomes are found in a human cell? How
many pair(s) of autosomes?
3. Read through "Behavior of Chromosome Sets in the Human Life Cycle" and "The Variety of Sexual Life
Cycles" on pp. 251-253. Use the figures on these pages to understand the alteration between meiosis and
fertilization in sexual life cycles. Be sure you can define each of those two terms, along with gametes,
zygote, haploid and diploid. How many chromosomes are found in a human haploid cell? in a human
diploid cell? Give an example of where you would find a human cell of each of these two types. What
would be the consequence for human reproduction (via the union of gametes) if gametes were produced
by mitosis instead of meiosis? Be sure you understand this.
4. Study the process of meiosis on pp. 254-255, and especially *note the comparison between meiosis and
mitosis as illustrated in Figure 13.9, p. 256. What are the critical differences between the two processes?
Notice that meiosis has a single replication of chromosomes, but two sets of cell divisions (called Meiosis
I and Meiosis II), resulting in a halving of the number of chromosomes in each of the daughter cells. If
you were observing a cell preparing to divide in one of the two ways (mitosis or meiosis), what is the first
point at which you would be able to tell that it was about to divide by meiosis instead of mitosis? What
would happen at that early point in the process of meiosis that would not happen in mitosis?
5. Explain what is meant by the terms synapsis and chiasmata. When do they occur? List the three events
that are unique to meiosis (as compared to mitosis) – note that all three happen during the first division,
Meiosis I.
6. Think about the mechanisms underlying sexual reproduction that generate genetic variation in
offspring. List, and describe thoroughly, the three sexual mechanisms that contribute to genetic variation
among offspring – a, b, and c. For a, answer this question: When a human sexual cell produces a gamete,
how many different possible ways are there to produce a gamete that contains only one of each of the 23
pairs of chromosomes? For b: How does crossing over (be sure you understand this term) produce one
chromosome that has some genetic material from each of the two parents? For c: Without considering
crossing over, how many different possible zygotes could be produced from a mating between a man and
a woman? Try to imagine what the mechanism of crossing over adds to this number…….
7. Finally, revisit Darwin's concept of natural selection, which is based on the fact that there is genetic
variation within a population. What are the two sources of this variation that you understand now,
remembering of course that both generate variation by chance?
BIOL 151L – Study Questions – Chapter 14 – Mendel and the Gene Idea – pp. 262-285
1. What is it about peas in general, and about the specific pea varieties and the specific pea traits that
Mendel chose to follow, that allowed him to do quantitative analysis of his results and to make the
conclusions he did? Be sure you can describe exactly how he did his experiments. What are the
parallels between his pea plants and fruit flies as an experimental system?
2. There are again important vocabulary words that you need to master to do this unit on genetics, and to
do the upcoming Genetics Problem Set. Be sure to learn, so that you are able to use, the following
terms: P (parental) generation, hybridization, F1 generation, F2 generation, alleles, dominant allele,
recessive allele, homozygous, heterozygous, genotype, phenotype, testcross, monohybrid, and dihybrid.
3. Explain Mendel’s “Law of Segregation” in relation to the 3:1 ratios (dominant trait : recessive trait) that
he saw among his F2 progeny. Be sure you can do the type of monohybrid cross illustrated in Fig. 14.5
through to the F2 generation. Be sure you understand how to set up the Punnett Square illustrated there.
4. What is the very specific meaning of “a testcross”? (Be sure your definition includes what genotype is
always used to do this type of cross.) Be sure you understand Fig. 14.7 and why you get either 100%
purple plants, or 50% purple, 50% white plants, after testcrossing the unknown purple plant.
5. Explain Mendel’s “Law of Independent Assortment” in relation to the results of the dihybrid cross
illustrated in Fig. 14.8 (and a 9:3:3:1 ratio). Be sure you know how to set up, and complete, the Punnett
Square shown in this Figure – very important.
6. Learn the basic principles of the laws of probability, including the multiplication rule and the addition
rule. To check your competence at this, do Concept Check 14.2 (p. 271), problems #1 and #2 (and check
your answers in the back of the textbook).
7. Learn the meaning of the following terms (all related to more complex types of inheritance patterns):
complete dominance, incomplete dominance, codominance. Explain how the allele that causes TaySachs disease can be considered either recessive, incompletely dominant, or codominant, depending on
how one examines the phenotype of an individual.
8. Explain how the human ABO blood group is an example of multiple alleles. Be sure you understand
Figure 14.11, P. 273.
9. What is a pedigree? What are the common symbols used there? What is a carrier?
10. Read about the recessively inherited disorders Tay-Sachs disease, cystic fibrosis, and sickle cell
disease. Which groups of people are especially affected by these? Are they the same for the three
disorders? Why or why not? What are examples of human disorders caused by dominantly inherited
alleles?
11. Read carefully the section on Genetic Testing and Counseling (pp. 279-281). What are some of the
ethical questions surrounding genetic tests to determine whether prospective parents are carriers of a
disease-causing, recessive allele? What is the difference between fetal testing versus newborn
screening? What is an example of a genetic disorder detected by newborn screening? How are the fetal
testing techniques of amniocentesis and chorionic villus sampling (CVS) done (see Fig. 14.18)?
BIOL 151L – Study Questions – Chapter 15 – The Chromosomal Basis of Inheritance – pp. 286-304
(Prepare for class Monday, October 19, 2009 – be sure work on these before class)
1. What exactly is the “chromosome theory of inheritance”? Study Figure 15.2 on page 287 and explain
how the behavior of chromosomes during meiosis accounts for the 9:3:3:1 ratio seen in the F2
generation of Mendel’s dihybrid crosses.
2. Figure 15.1 on page 274 shows a yellow fluorescent dye that highlights a particular gene on a certain
human chromosome. Why are there four spots visible?
3. As your textbook says, the first solid evidence associating a specific gene with a specific chromosome
came from T.H. Morgan’s work with the mutant white allele (= w, versus the wild type allele = w+)
in fruit flies. What was the first observation he made that this gene was behaving differently from
others he had studied (from doing a two-generational cross of a male white-eyed mutant fly with a
wild type female fly)? Set up and do the cross illustrated in Figure 15.4 (p. 289) yourself. Do you
now understand the genetics behind the strange observation that T.H. Morgan made in his original
cross?
4. Notice (e.g. in Figure 15.7) the special notation that is used to do crosses with sex-linked genes ( i.e.
genes located on either of the sex chromosomes; here we are working with a gene located on the X
chromosome, so it is X-linked [and note that there is no corresponding gene present on the Y
chromosome, which is much smaller than the X chromosome]). Be sure to notice the difference
between the terms “sex-linked” (or “X-linked”) versus “linked” (described in the next section). Do
for yourself the crosses illustrated in Figure 15.7 and be sure you understand why males are more
likely than females to show the phenotype of a recessive X-linked gene. There are Genetics Problems
you can try at the end of this chapter – do problems #1-3 on p. 303 and check your answers..
5. What does it mean to say that two genes are linked? Study the cross illustrated in Figure 15.9 (page
293) and Figure 15.10 (p. 295). First, notice which combinations of alleles for the two genes under
examination are classified as “parental,” and which are classified as “recombinant.” Why are there
more parental than recombinant phenotypes observed among the offspring of the testcross illustrated
in these figures? Second, why are there any recombinant offspring observed at all, given these two
genes are on the same chromosome (i.e. linked) and therefore travel together? Be sure you
understand the concept of crossing over, which accounts for recombination between linked genes.
Study Figure 15.10 on page 295 (and review Fig. 13.12 on p. 259) to be sure you understand this.
6. One of Morgan’s students, A.H. Sturtevant, proposed that one could map the relative distances between
linked genes (those on the same chromosome) by determining the recombination frequency observed
between them during a genetic cross. He reasoned that the farther apart two genes are, the higher the
probability that a crossover will occur between them and therefore the higher the observed
recombination frequency. How did he define one “map unit” of distance between 2 linked genes?
Study Figure 15.11 on page 296 to understand how a “linkage map” of three genes on one
chromosome is constructed. Do Genetics Problems #4 on page 303 ands check your answer.
7. Study Figure 15.13 (p. 297) to see two different ways by which nondisjunction can occur during
meiosis. What does this term mean? What is a common human syndrome, involving chromosome
21, that most often occurs due to nondisjunction? What is an example of a syndrome in humans
caused by nondisjunction of human sex chromosomes?
BIOL 151L – Study Questions – Chapter 16 – The Molecular Basis of Inheritance – pp. 293-308
(prepare for class Friday, October 23, 2009)
1. In the 1940's, scientists knew that chromosomes consisted of DNA and protein. Given the great amount, and
the diversity, of heritable information known to be passed from parent to offspring, most researchers thought that
proteins must be the genetic material. Why do you think they thought that? (Hint: How many different building blocks
are used in the synthesis of proteins? How many different building blocks are used in the synthesis of DNA?)
2. Describe the experiments with Streptococcus pneumoniae done by F. Griffith in 1928 in which he
demonstrated transformation. What was "transformed" from what to what? What were the controls he did (i.e. what
components of the experiment did he test separately, and what happened)? What was it about his experiments that
hinted that protein was not the transforming agent? About 15 years later, in 1943, Oswald Avery finally demonstrated
that DNA was the transforming agent. How did he show this?
3. In 1952, Hershey and Chase provided evidence that viral DNA, not protein, can direct the synthesis of
hundreds of progeny virus particles inside bacterial cells; thus, DNA is the genetic material of these viruses, called
bacteriophages (or, phages, for short). Notice that the scientists used either radioactive sulfur (sulfur is found only in
proteins, not nucleic acid) or radioactive phosphorus (found in DNA, not protein) to selectively label either the protein
or the DNA of the infecting phages in different experiments. Following an incubation time allowing the phages to
inject their genetic material into the bacterial cells, how did the scientists separate the parts of the phage still outside the
cell from the genetic material inside the cell? How did they determine which part of the phage had entered the cell and
which part did not (be sure to use the words "supernatant" and "pellet" in your answer)? Why did they conclude that it
is the phage DNA that is the genetic material?
4. Watson and Crick put together several pieces of data in order to come up with their model of the doublehelical structure of DNA. What clues did each of the following provide toward solving the puzzle?
a) Chargaff's data that in the DNA from an organism, the % of A bases = the % of T bases, and the % of G
bases = the % of C bases
b) The X-ray diffraction photo of DNA taken by Rosalind Franklin (see Fig. 16-6)
c) The purines (A and G) are twice as wide as the pyrimidines (C and T).
Review the three-part composition of a nucleotide (see Fig. 16-5). In imagining the double-helix of DNA as a twisted
ladder, what forms the side-ropes of a twisted ladder model and what forms the rungs?
5. As noted in the textbook, and of course by Watson and Crick themselves, the beauty of the model of DNA
as a double helix (with particular base-pairings) was that the structure suggested the basic mechanism of DNA
replication. What is this basic concept? (See Fig.16-9 for help here.) To what does the term "semiconservative"
replication refer? Study the three models of DNA replication as presented in Figure 16-10. How did the famous
Meselson-Stahl experiment support the idea that the semiconservative model was the correct one?
6. In the double-stranded DNA molecule, replication begins at an origin of replication and proceeds from there
in both directions, with the two strands of the double-helix opening at two replication forks to allow the synthesis of the
new strands of DNA. At the replication fork, both strands must serve as templates that direct the synthesis of the two
daughter strands. Describe the role of each of the following proteins in the synthesis of the new leading strand:
helicase, primase, DNA polymerase.
Because the two template strands are antiparallel (what does that mean?), the new lagging strand must be
synthesized as a series of Okazaki fragments. Describe the role of the following proteins in synthesis of the lagging
strand: primase, two different DNA polymerases, DNA ligase. Note that DNA polymerases not only synthesize the
new Okazaki fragments but also replace the RNA primer with DNA before DNA ligase can do its job (what?).
7. DNA is proofread as it is synthesized, and it can be repaired after DNA strand synthesis is complete if an
error is detected later (e.g. a mismatch, or a damaged nucleotide). What enzyme(s) proofreads each nucleotide as it is
added to the growing strand of DNA? What happens if an error is detected at that stage? How does nucleotide excision
repair work, and when does it occur? What is the source of the correct information used in this type of repair? Note that
hereditary defects in different proteins involved in repair are associated with two forms of cancer –colon cancer and
xeroderma pigmentosum).
8. What is a telomere and where is it found? What is the role of the enzyme telomerase, in general (no
specifics)?
9. What is chromatin? What are histones and why are they important? What are nucleosomes? To what do
each of the following levels of chromosome packing refer: "beads on a string," 30-nm fiber, looped domains? Be sure
to study both the drawings and the actual electron microscope photos of Figure 16.21 (pp. 320-321) that show the
stages of chromatin packing as a chromosome condenses to its most compact form -- that seen at metaphase.
**For a good review, do Self-Quiz problems (p. 324) #1-6, and 8.
BIOL 151L – Study Questions – Chapter 17 – From Gene to Protein – pp. 325-350
1. Explain briefly what Archibald Garrod meant in 1909 by an “inborn error of metabolism.” What was his
idea about the connection between genes and enzymes in human?
2. Review the following, which your book calls the “molecular chain of command" (p. 328):
DNARNAprotein (also called "The Central Dogma of Molecular Biology"). What is the process of
transcription? Where in the cell does it take place? What is the product of transcription? What is
translation, and where in the cell does it take place? Transcription and translation are said to be “coupled” in
prokaryotes – what does that mean (see Fig. 17.3a)? Why are they not coupled in eukaryotes? Explain these
last two sentences in terms of the differences in the structure of the prokaryotic versus the eukaryotic cell (and
see Figure 17.3 in your text – very important). Be sure that you learn these two underlined (and in bold)
vocabulary words above – they are some of the most important in molecular biology, and are easily confused,
as well as used very often!
3. What is a codon in a messenger RNA (mRNA) molecule? How many nucleotides are in a codon that codes
for one amino acid? How many possible codons are there, given that there are four different nucleotides?
How many of these code for one of the twenty amino acids? What is the redundancy (p. 330) in the code?
How many of the codons code for stop codons, and what are these? How many start codons are there?
Explain what the reading frame of a messenger RNA is. How many reading frames are possible in a region of
a messenger RNA? Finally, in the mRNA molecule given below, circle the codons and then use the
"Dictionary of the Genetic Code" on page 330 to determine what amino acid each codes for:
5' A U G C C A G G A U C C U A A 3'
4. Taking a closer look at transcription, what enzyme synthesizes the mRNA molecule by making a
complementary copy of one strand of the DNA? (Note that this mRNA molecule is complementary and
antiparallel to the DNA template strand.) What is the signal sequence on the DNA template strand that tells
the RNA-synthesizing enzyme where to start? To which end (5' or 3') of the growing RNA strand are
nucleotides added? How does the RNA-synthesizing enzyme know when to stop copying the DNA into RNA?
5. In eukaryotes, but not prokaryotes, RNA is modified after transcription and before it leaves the nucleus for
the cytoplasm, where the ribosomes are located. (Why doesn't this happen in a prokaryotic cell?) What
modifications are made to each end of the eukaryotic mRNA, and what functions do these modifications
serve?
6. What is RNA splicing? What are introns and exons?. What is the function of the spliceosome (its name
helps here)? Notice that some RNAs that get spliced do it without protein enzymes, but rather through
ribozymes (= RNA "enzymes"). In fact, the enzyme that is responsible for forming the peptide bonds between
amino acids in the growing polypeptide chain on a ribosome is actually an RNA molecule within the ribosome!
7. Recall that the process of protein synthesis, translation, involves the "translation" from one language (that
of nucleic acids = the mRNA) into another (the amino acids that make up a protein). The mRNA molecule is
made up of codons that carry the message and get translated. What is the "interpreter" in this process? Note
that individual transfer RNAs (tRNAs) bring individual amino acids to the ribosome, the site of protein
synthesis. How do these tRNAs associate the amino acid that each carries with a particular codon on the
mRNA? One analogy used is that a tRNA molecule is like a flashcard with a "nucleic acid word" (anticodon)
on one side and a "protein word" (amino acid) on the other (attached to the 3’ end of the tRNA). Also, notice
that the anticodon on the tRNA binds, using complementary base-pairing, to a codon on the mRNA (e.g. an
AAA anticodon will pair with a UUU codon). Notice the structure of a tRNA – it is a small molecule of RNA
that folds into a cloverleaf structure that is stabilized by base pairing within the molecule itself (similar to the
way a protein has a globular, tertiary structure held together by H bonds, ionic bonds, etc.).
(continued next page)
8. What enzyme is responsible for attaching an amino acid to its correct tRNA? What fits into the active site
of this enzyme? How many different types of this enzyme are there in a cell? Why? What would be
considered the product of this enzymatic reaction?
9. What are the two components that make up all ribosomes? The ribosome can be thought of as a docking
platform where the mRNA and the tRNAs come together for the process of translation to take place. Given
this, what are the three binding sites on the ribosome (what binds to each of them)? Study Figure 17-16 and
note that a tRNA carrying the growing Polypeptide chain binds to the P site, while the incoming tRNA
carrying the next Amino acid to be added binds to the A site. (Do note that the structure of prokaryotic versus
eukaryotic ribosomes are very similar, yet different enough that there are drugs that paralyze prokaryotic but
not eukaryotic ribosomes – i.e. tetracycline and streptomycin, which are taken by humans to combat bacterial
infection.)
10. Note that in the process of initiation of translation (Fig. 17-17), the three types of RNA in a cell are
brought together – the mRNA, which carries the instructions for making the protein, the initiator tRNA, which
brings the first amino acid needed to build the protein, and the ribosomal RNAs (rRNAs), which are a main
component of the ribosome (along with many proteins). Note what binds to what and where in this complex.
11. Go over the three stages of elongation (during translation) – study Figure 17-18. 1) Codon recognition -An incoming tRNA carrying the next amino acid to be added to the growing polypeptide chain hydrogen
bonds through its anticodon to the codon on the mRNA that is currently positioned in the A site of the
ribosome. 2) A peptide bond is formed between the incoming amino acid and the end of the polypeptide chain
on the tRNA in the P site. The polypeptide chain is transferred to the tRNA in the A site during this process.
3) Translocation – the ribosome moves one codon down the mRNA, positioning the next codon to be read into
the A site, and moving the tRNA with the growing polypeptide chain into the P site. This step requires energy,
obtained through the hydrolysis of GTP (an energy source similar to ATP).
12. What happens at the termination step of protein synthesis (Fig. 17-19)? What are the stop codons, and
where do they have to be to bring about termination? What does a release factor do?
13. What is a polyribosome (see Figure 17-20)?
14. What kinds of things happen to a protein during posttranslational modification? Give an example.
15. What is a signal sequence found at the beginning of some proteins? What is its function? Note (see Fig.
17-21) how this targets both the protein, and the ribosome on which it is being made, to the surface of the
endoplasmic reticulum, thus turning a free ribosome into a bound ribosome (remember those terms from
studying cell structure?). Where does the newly made protein end up?
**16. What is a mutation? What is a point mutation? What is the genetic basis for sickle-cell disease (see
Figure 17-22)? What is a base-pair substitution? In terms of a base-pair substitution, what is the difference
between a silent mutation and a missense mutation? What is a nonsense mutation? How is it that insertions or
deletions of one or two nucleotides change the reading frame of the genetic message = a frameshift mutation?
Why is this such a serious mutation? Will an insertion of three nucleotides cause a frameshift mutation?
Why? Note that there are many physical and chemical agents that interact with DNA to cause mutations -these are called mutagens, and obviously can be very dangerous.
**17. In conclusion and in summary, study Figure 17-25 for an overview of transcription and translation in a
eukaryotic cell.
**Do use the Summary of Key Concepts at the end of the chapter (p. 349-350) to help you review the
information in this chapter – there's a lot of it, and it’s critically important!
BIOL 151L – Study Questions – Chapter 18 – Regulation of Gene Expression – pp. 351-380
Part I
Friday, November 6 – Monday, November 9, 2009
1. Why is it important that bacteria be able to regulate their metabolism to match particular environments or
circumstances? How can cells regulate the activity of an enzyme already present in a cell (see Fig. 18.2). What
is feedback inhibition? Why is it also important that bacteria be able to regulate whether particular genes (i.e.
a gene that encodes a particular enzyme) are “off” or “on” at particular times or under particular
circumstances?
2. What is an operon? What are the three component parts (page 352 and Fig. 18.3), and what is the function
of each? To which does RNA polymerase bind to begin transcription? To which does the repressor bind, and
what is the consequence of that binding?
3. We will study the regulation of the trp operon and the lac operon as examples of gene regulation in
bacteria. Study the structure of the trp operon (Fig. 18.3). What is the end product of the enzymes made from
the genes of that operon? Notice that this is a product often needed by the cell, and as a result this operon is
normally switched ON in the cell. However, there is a way to turn off the operon when there is enough of the
end product already present in the cell. How does that happen? What is the corepressor, and how does it shut
off the operon? Notice that because this operon is normally ON, but can be switched off, it is an example of a
repressible operon.
4. On the other hand, the lac operon (see Fig. 18.4) is considered an inducible operon because it is normally
switched OFF in the cell, but can be switched on under certain conditions. When the structural genes of the lac
operon are expressed, they make enzymes that allow bacteria to break down and use the sugar lactose as an
energy source. When lactose is not available, the lac operon is turned off (the genes are not transcribed by
RNA polymerase) – how is this accomplished? What is the role of the repressor? When lactose is present, the
genes are expressed – how is this accomplished? What is the inducer, and what is its role? How is the
presence or absence of lactose monitored? Overall, this is an example of negative control, where the binding
of a molecule (the repressor) switches off the operon.
5. The same operon provides an example of positive control, where the binding of a molecule turns on the
operon. In this specific case, the system allows the operon to monitor whether an alternative energy source,
glucose, is available. If so, it is "cheaper" for the bacterium to use glucose instead of lactose and,
consequently, the lac operon should remain turned off. Describe how this positive regulation of the lac
operon works (see Fig. 18.5). What molecule is it whose binding turns on the operon? How does the
concentration of glucose in the cell affect this binding?
6. Your text talks about the two types of regulation of the lac operon as an on-off switch and a volume control
(p. 355). Which is which?