DNA-Protein
Explain why the genetic code is described as “redundant but not ambiguous.”
Multiple codons code for the same amino acid (redundant), but each codon codes for only one amino acid (not ambiguous).
Which checkpoint ensures DNA is fully replicated before mitosis begins?
G2 checkpoint
Why does mitosis maintain chromosome number while meiosis reduces it?
Mitosis separates sister chromatids; meiosis I separates homologous chromosomes.
Name three enzymes involved in DNA replication.
Helicase, DNA polymerase, ligase (also primase acceptable).
Loss of contact inhibition causes cells to do what?
Continue dividing even when touching neighboring cells.
The mutated Foxp3 sequence contains a premature stop codon. Identify the mutation type and justify your answer.
Nonsense mutation; a codon was changed into a STOP codon, truncating the protein.
Describe how proto-oncogenes differ from tumor suppressor genes in normal function.
Proto-oncogenes promote cell division; tumor suppressors inhibit division or repair damage.
Crossing-over increases genetic variation by doing what at the molecular level?
Exchanging DNA segments between homologous chromosomes, creating new allele combinations.
Why does DNA polymerase reduce—but not eliminate—mutation rates?
It proofreads, but occasional errors escape correction.
Apoptosis protects the body by doing what?
Eliminating damaged or abnormal cells.
If a single nucleotide deletion occurred near the beginning of the Foxp3 coding sequence, predict how the resulting amino acid chain would differ from the original.
Frameshift; all downstream codons would change, likely producing a drastically altered and nonfunctional protein.
Explain how a mutation converting a proto-oncogene into an oncogene promotes cancer.
It becomes overactive or constantly “on,” stimulating uncontrolled cell division.
Predict the consequence if crossing-over did NOT occur during meiosis.
Reduced genetic variation; fewer recombinant chromosomes.
Explain how an error during DNA replication could alter gene expression without changing the amino acid sequence.
Silent mutation or mutation in regulatory region affecting transcription levels.
A tumor suppressor gene mutation is inherited. Why might cancer still develop later in life instead of immediately?
A second mutation (“second hit”) must occur in the other allele.
Explain why a mutation in a tumor suppressor gene often requires loss of both functional alleles to significantly increase cancer risk.
Tumor suppressors are typically recessive at the cellular level; one functional copy can often still regulate the cell cycle (two-hit hypothesis).
If p53 detects DNA damage but apoptosis does not occur, identify two possible molecular failures.
p53 mutation, apoptosis pathway mutation, checkpoint failure, or signaling pathway disruption.
A cell undergoes nondisjunction during meiosis I. Predict the chromosome number in the resulting gametes.
All four gametes abnormal (two n+1, two n−1)
Predict how a mutation in a promoter region differs from a mutation in a coding region.
Promoter mutation affects transcription level; coding mutation affects protein structure.
Explain how mutations in DNA repair genes increase the mutation rate in other genes.
Repair mechanisms fail, allowing replication errors to accumulate across the genome.
Foxp3 is located on the X chromosome. Predict why mutations in this gene may have different effects in males versus females.
Males have one X chromosome (XY), so one mutation causes full loss of function. Females have two X chromosomes (XX), so one functional copy may compensate (depending on X-inactivation).
A biopsy shows rapid cell division, no contact inhibition, and accumulation of DNA errors. Identify which regulatory systems have likely failed and explain how they interact.
Tumor suppressors (like p53), checkpoints, apoptosis mechanisms, and contact inhibition. Loss of these controls allows damaged cells to continue dividing.
Compare the role of spindle fibers in mitosis and meiosis I. Why is their attachment pattern critical in meiosis I?
In mitosis, spindle fibers separate sister chromatids. In meiosis I, they separate homologous chromosomes. Incorrect attachment causes nondisjunction.
Explain how replication errors combined with checkpoint failure create a “snowball effect” in cancer development.
DNA damage accumulates, mutations increase, regulatory genes become altered, accelerating uncontrolled division.
Design a pathway explaining how a single point mutation in a checkpoint gene could eventually lead to metastatic cancer.
Mutation → checkpoint failure → damaged cells divide → additional mutations accumulate → tumor formation → invasion → metastasis.