Cycle 6

Question 1

🃏 Q: What are the two types of complexity?

Answer 1

✅ A: Morphological complexity (cell types, tissues, organs) and biochemical complexity (metabolic pathways).

Question 2

🃏 Q: Why are eukaryotes more complex than prokaryotes?

Answer 2

✅ A: They have more energy due to oxygen and mitochondria, enabling larger genomes and more cell types.

Question 3

🃏 Q: Why don’t prokaryotes have larger genomes?

Answer 3

✅ A: Energy limitations prevent genome expansion; they must keep gene density high for efficiency.

Question 4

🃏 Q: What caused the GOE?

Answer 4

✅ A: Cyanobacteria evolved oxygenic photosynthesis, using water as an electron donor and releasing O₂.

Question 5

🃏 Q: How did the GOE lead to increased complexity?

Answer 5

✅ A: Oxygen enabled aerobic respiration, allowing cells to generate much more ATP, supporting genome expansion and new cell types.

Question 6

🃏 Q: What is the endosymbiotic theory?

Answer 6

✅ A: Mitochondria and chloroplasts originated as free-living bacteria engulfed by an ancestral anerobic archea cell.

Question 7

🃏 Q: What is the evidence for the endosymbiotic origin of mitochondria and chloroplasts?

Answer 7

✅ A: Own genome, double membranes, reproduce independently, have bacterial-like ribosomes, and conduct electron transport.

Question 8

🃏 Q: Why did mitochondrial and chloroplast genomes shrink?

Answer 8

✅ A: Redundant genes were lost, and others moved to the nucleus via horizontal gene transfer (HGT).

Question 9

🃏 Q: What is HGT?

Answer 9

✅ A: Movement of genes between genomes (e.g., from mitochondria/chloroplasts to the nucleus).

Question 10

🃏 Q: Why does HGT happen in mitochondria and chloroplasts?

Answer 10

✅ A: The nucleus must regulate cell functions efficiently by controlling respiration and photosynthesis.

Question 11

🃏 Q: Why haven’t all organelle genes moved to the nucleus?

Answer 11

✅ A: Some genes (e.g., electron transport proteins) must stay in organelles due to high damage rates and need for rapid synthesis.

Question 12

🃏 Q: How can we detect HGT?

Answer 12

✅ A: Using DNA hybridization:

If a gene is only in mtDNA → No HGT
If a gene is only in nuclear DNA → HGT has occurred
If a gene is in both → Gene is in transition

Question 13

🃏 Q: How do proteins coded by nuclear DNA reach mitochondria/chloroplasts?

Answer 13

✅ A: They contain a signal peptide, which directs them to the correct organelle.

Question 14

🃏 Q: What happens to the signal peptide after a protein reaches its destination?

Answer 14

✅ A: It is cleaved off, allowing the protein to fold properly.

Question 15

🃏 Q: What is the three-domain vs. two-domain debate?

Answer 15

✅ A: Traditional: Bacteria, Archaea, and Eukaryotes.
Newer view: Eukaryotes evolved from Archaea (Asgard group).

Question 16

🃏 Q: What does it mean that eukaryotic cells are chimeras?

Answer 16

✅ A: They contain genes from both Archaea (information processing, structure) and Bacteria (metabolism, endosymbionts).

Question 17

🃏 Q: What is surprising about eukaryotic membrane lipids?

Answer 17

✅ A: Despite eukaryotic cells originating from Archaea, their membrane lipids are bacterial in origin.

Question 18

🃏 Q: Why does Chlamy have three genomes?

Answer 18

✅ A: It has separate nuclear, mitochondrial, and chloroplast genomes, each requiring its own transcription/translation machinery.

Question 19

Q: What is an antibiotic?

Answer 19

A: An antibiotic is an organic compound that can either kill bacteria or inhibit bacterial growth. Many occur naturally, while others have been developed synthetically.

Question 20

Q: Why is antibiotic resistance considered one of the biggest crises in healthcare?

Answer 20

A: Antibiotic resistance occurs when bacteria evolve mechanisms to resist the effects of drugs that once killed them or inhibited their growth, making infections harder to treat.

Question 21

Q: Who discovered penicillin, and how did it happen?

Answer 21

A: Penicillin was discovered by Alexander Fleming around 100 years ago. He noticed a petri dish with bacteria contaminated with the fungus Penicillium notatum, where bacteria near the fungus were killed, leading to the discovery of penicillin’s antibacterial properties.

Question 22

Q: What are some common bacterial infections treated with antibiotics?

Answer 22

A: Infections caused by Staphylococcus aureus, Mycobacterium tuberculosis, Streptococcus pneumoniae, Treponema pallidum (syphilis), and more.

Question 23

Q: Why are bacteria harmful?

Answer 23

A: Bacteria have a fast growth rate (doubling every 20 minutes at 37°C), and they can produce toxins that harm immune cells. If the toxins reach high enough levels, they can kill cells.

Question 24

Q: What is a plasmid in bacteria?

Answer 24

A: A plasmid is non-chromosomal DNA that doesn’t code for essential functions but plays a crucial role in the spread of antibiotic resistance.

Question 25

Q: What is the difference between Gram-positive and Gram-negative bacteria?

Answer 25

Gram-positive: Stains readily and has one membrane. Gram-negative: Does not stain readily, has two hydrophobic membranes, and often contains porins that allow selective transport.

Question 26

Q: Why are Gram-negative infections harder to treat with antibiotics?

Answer 26

A: Gram-negative bacteria have two membranes that act as barriers, preventing antibiotics from entering easily.

Question 27

Q: How do antibiotics like penicillin work?

Answer 27

A: Penicillin interferes with cell wall biosynthesis by inhibiting the enzyme transpeptidase, preventing the linking of polysaccharide sheets in the bacterial cell wall, which is necessary for bacterial division.

Question 28

Q: What is the difference between reversible and irreversible competitive inhibitors?

Answer 28

A: Irreversible competitive inhibitors, like penicillin, bind to the active site of an enzyme permanently, rendering it useless. Reversible inhibitors can bind and unbind.

Question 29

Q: How do sulfonamides work as antibiotics?

Answer 29

A: Sulfonamides inhibit folate biosynthesis in bacteria, which is necessary for their growth, while humans obtain folate from their diet.

Question 30

Q: How do antibiotics like kanamycin and tetracycline affect bacteria?

Answer 30

A: They target bacterial protein synthesis by binding to bacterial ribosomes, which are structurally different from human ribosomes, thus preventing bacteria from making proteins needed for growth.

Question 31

Q: What is the action mechanism of ciprofloxacin?

Answer 31

A: Ciprofloxacin interferes with DNA gyrase, an enzyme involved in DNA replication, preventing the bacterial DNA from unwinding and replicating.

Question 32

Q: Why don’t antibiotics like penicillin harm human cells?

Answer 32

A: Humans don’t have cell walls, so antibiotics like penicillin, which target cell wall biosynthesis, don’t affect human cells. Additionally, mitochondria in human cells grow slowly compared to rapidly dividing bacteria.

Question 33

Q: How does antibiotic resistance spread in bacteria?

Answer 33

A: Resistance can spread through random mutations or horizontal gene transfer, such as conjugation, where plasmids carrying resistance genes are transferred between bacterial cells.

Question 34

Q: What are some common mechanisms of antibiotic resistance? (4)

Answer 34

1) Porin downregulation: Reduces antibiotic influx. 2) Target site modification: Changes the target of the antibiotic. 3) Active efflux: Pumps the antibiotic out of the cell. 4) Target bypass: Bacteria produce alternative enzymes with the same function as the target enzyme.

Question 35

Q: What is Teixobactin and why is it significant?

Answer 35

A: Teixobactin is an antibiotic discovered in 2015 that prevents cell wall biosynthesis. It is effective against S. aureus and has shown no resistance to date, making it a promising solution to antibiotic resistance.

Question 36

Q: Why don’t bacteria develop resistance to Teixobactin?

Answer 36

A: Teixobactin targets two different pathways in cell wall biosynthesis, making it difficult for bacteria to develop resistance to it. Additionally, resistance mutations have not been observed.