Tutorial 1

12/09/23
1. Mutations are mistakes in the DNA that change the genetic plan from that of the previous generation. Imagine a shoe
factory in which your favorite brand of sneakers is constructed every day on an assembly line. Each shoe is exactly the same
as the one before it and as the original design.
 Would you expect mistakes (i.e., unintentional changes) in copying the shoe design in a single pair of shoes to lead to
improvements in the shoes produced? Explain your answer.
 What would happen if these unintentionally made new shoes had no soles? How many people would purchase them?
How many people would want the original version of the shoe?
 What would happen if the unintentionally made new shoes had improved arch support and comfort? Would more or
fewer people purchase them? Would more or fewer people want the original version of the shoe?
 What would happen if the unintentionally made new shoes were orange instead of white? Would more or fewer people
purchase them? Would more or fewer people want the original version of the shoe?
 How can you apply this idea to cells?
 How can you apply this idea to the history of the cell from ancestral to present times?
 What role does the environment play in the process of evolution?

Mutations are essential for driving evolution, and their effects on an organism's fitness depend on whether they are neutral,
beneficial, or harmful, much like the different effects of changes in shoe design. The environment acts as the ultimate arbiter,
influencing the prevalence of specific genetic traits in populations.
2. The antibiotic streptomycin inhibits protein synthesis in bacteria. If this antibiotic is added to a culture of animal
cells, protein synthesis in the cytosol continues normally. However, over time, the population of mitochondria in the
cell becomes depleted. Specifically, scientists observe that the protein-synthesis machinery inside the mitochondria
is inhibited. Explain this observation based on what you know about the origins of the modern eukaryote.

 Considering the postulated origin of mitochondria from an ancient aerobic bacterium that was engulfed by an
ancient eukaryote, it is plausible that antibiotics designed to inhibit bacterial protein synthesis could also
impede this process in mitochondria. This likelihood arises from the preservation of mitochondrial features
reminiscent of their bacterial ancestors, including ribosomes and protein synthesis machinery. Therefore,
antibiotics like streptomycin, which specifically target bacterial ribosomes, may equally affect mitochondrial
protein synthesis. This shared vulnerability underscores the evolutionary connection between mitochondria
and bacteria and emphasizes the significance of caution when using such antibiotics, as their impact on
mitochondria can disrupt essential cellular functions.
3. What do you expect to observe if, in a new experiment, animal cells are treated with diphtheria toxin, a
compound known to block cytosolic protein synthesis but that does not have any impact on bacterial growth?

 We would expect that although cytosolic protein synthesis would stop, mitochondrial protein synthesis should
still occur normally (at least for a little while). This result would lend further support to the idea that
mitochondria are derived from a noneukaryotic organism. If this were not the case, these compounds would
be expected to affect protein synthesis at both locations.
4. List four characteristics of mitochondria that support the endosymbiotic hypothesis.
1. Circular chromosomal DNA which is similar to prokaryotes.
2. Mitochondria and bacteria are similar in size.
3. Binary fission is used as their mode of replication.
4. The inner membrane contains ATP synthase just like bacteria.
5. You fertilize egg cells from a healthy plant with pollen (which contains the male germ cells) that has been treated
with DNA-damaging agents. You find that some of the offspring have defective chloroplasts, and that this
characteristic can be passed on to future generations. This surprises you at first because you happen to know that
the male germ cell in the pollen grain contributes no chloroplasts to the fertilized egg cell and thus to the
offspring. What can you deduce from these results?

• Your results show that not all the information required for making a chloroplast is encoded in the
chloroplast’s own DNA; some, at least, must be encoded in the DNA carried in the nucleus. The reasoning is
as follows: Genetic information is carried only in DNA, so the defect in the chloroplasts must be due to a
mutation in DNA. But all the chloroplasts in the offspring (and thus all the chloroplast DNA) must derive
from those in the female egg cell, since chloroplasts only arise from other chloroplasts. Hence, all the
chloroplasts contain undamaged DNA from the female parent’s chloroplasts. In all the cells of the offspring,
however, half of the nuclear DNA will have come from the male germ-cell nucleus, which combined with the
female egg nucleus at fertilization. Since this DNA has been treated with DNA-damaging agents, it must be
the source of the heritable chloroplast defect. Thus, some of the information required for making a
chloroplast is encoded by the nuclear DNA.
6. Most cells use glucose for ATP synthesis, but some cells will preferentially use other fuel molecules for ATP synthesis,
like fatty acids or amino acids. The cells of the outer segment of the retina are almost totally devoid of mitochondria and
rely only on glucose to generate ATP. Explain why retinal cells are dependent on glucose and cannot use fatty acids or
amino acids for ATP synthesis. Explain how retinal cells use glucose for energy by describing the pathway(s) and
molecules involved.

Why retinal cells are dependent on glucose: How retinal cells use glucose for energy:

o Amino acids can’t be converted into acetyl o Glucose  pyruvate through glycolysis, 2
CoA because that occurs in the ATP
mitochondrial matrix. o Pyruvate  lactic acid through
o Amino acid  pyruvate in the cytoplasm fermentation, regeneration of NAD+
does not generate ATP.
o Fatty acids can’t be converted into acetyl
CoA because that occurs in the
mitochondrial matrix.
o Glucose can go through glycolysis in the
cytoplasm which generates 2 ATP/glucose.
7. Although ATP and NADH are both important activated carrier molecules, ATP hydrolysis provides the direct
molecular energy for most biochemical reactions. Why do the mitochondria also need to generate high levels of
NADH?

 NADH is a versatile activated carrier molecule, serving as a cofactor for numerous enzymes involved in
catalyzing redox reactions. In addition to its role as a cofactor, NADH plays a crucial role by donating
electrons to the electron-transport chain, an indispensable process in the generation of ATP.
8. What are the similarities and differences between mitochondria/oxidative phosphorylation and
chloroplasts/light reactions?

• Shared Features:
 Both contain DNA and ribosomes.
 Both are surrounded by a double membrane.
 Both generate ATP.
 Both rely on an electron transport complex and ATP synthase.
• Differences:
 Different terminal electron receptors (O2 in cellular respiration and NADP+ in the light reactions).
 Oxygen (O2) is required in cellular respiration and produces CO2 as a by product, while the light
reactions produce O2 and utilize CO2 in the Calvin cycle.
 Cellular respiration occurs in all living organisms, while photosynthesis is limited to plants, algae, and
some bacteria.
 The process of photosynthesis utilizes ATP, whereas cellular respiration produces ATP.
9. The chemical paraquat is used as an herbicide (plant killer). It is highly regulated in both the United-States and in
Canada due to its toxicity to humans. Exposure to paraquat has also been linked to Parkinson’s disease in humans. Briefly
research the mechanism of action of paraquat and explain why it is toxic to both plants and humans and why it may cause
symptoms that resemble Parkinson’s.

 Paraquat interferes with electron transfer.

 Plants: accepts electrons from photosystem I and transfers them to oxygen. This produces reactive oxygen species. Paraquat
can then accept more electrons from photosystem I, this process prevents the production of NADPH. Reactive oxygen species
destroy cells.
 Humans: diverts electrons from complex I in humans with similar effects. Lethal.
o An increase in ROS in mitochondria has been linked to Parkinson’s disease. Paraquat causes an increase in ROS, thus
paraquat may potentially cause symptoms that resembled Parkinson’s disease.
10. Human infants have a much larger portion of brown adipose tissue than adult humans. It was found that the mitochondria in
brown adipocytes (brown fat cells) have a novel protein in the inner mitochondrial membrane. This protein, called the
uncoupling protein (UCP), was found to transport protons from the intermembrane space into the matrix. What is the impact of
UCP on oxidative phosphorylation in the mitochondria of brown fat?

 A protein that transports protons into the mitochondrial matrix would diminish the proton gradient. Without the
proton gradient, ATP will not be generated. However, the electron-transport chain can still work, if oxygen is present.
The UCP, therefore, is a biological uncoupler of the oxidative phosphorylation process. The electron-transport chain
will run in a futile cycle that does not convert the energy from redox reactions into chemical energy (ATP) but
instead releases this energy as heat.