In Kevin's case, a specific kind of mutation in the opsin gene resulted in the premature termination of
the translation process. This resulted in shorter opsin protein than usual. What specific mutation could
have caused this? - ✔✔Nonsense mutation
The nonsense mutation that causes Kevin's color blindness could have resulted from a malfunction of -
✔✔DNA polymerase
One strand of chromosome 2 has a DNA sequence that consists of: 5'- AAG CGG TAC GTA -3'. What will
be the sequence of the complementary DNA strand? - ✔✔5' - TAC GTA CCG CTT -3'
A woman is homozygous for an abnormal gene on Chromosome 2 that codes for an autosomal
dominant disease. This means that she - ✔✔will have the disease
A man and woman with both type O blood have 4 children, what will be the blood types of their
children? - ✔✔100% type O
, A couple has 6 children, 4 girls and 2 boys, all of whom have prominent chin dimples. If only the mother
has a prominent chin dimple, what is the likely inheritance pattern for the chin dimple? - ✔✔autosomal
dominance
Epigenetics: access to the promoter region of a gene by transcription factors is affected, environmental
stimuli control gene expression, and gene expression is influenced by chemical modifications of the DNA
and/or histone proteins - ✔✔True
Red green colorblindess - ✔✔is due to a mutation in the opsin gene
The LCT gene codes for Lactase, which is responsible for the breakdown of lactose. How is the Lactase
activity increased? - ✔✔the presence of lactose causes nucleosomes to separate, exposing the LCT gene
Histone proteins can be chemically modified by addition of methyl group. As a result, nucleosomes
pack tightly and the process of transcription is decreased at those DNA sites - ✔✔True
When the wrong nucleotide is added to a newly forming DNA strand during DNA replication: -
✔✔distortion of the double helix retains its shape due to the pairing of A with T and G with C
Mutation to the DNA strand that consists of a nucleotide sequence: 5'- CTG ACG TAT CTT AAT -3' -
✔✔5'-CTG ACG TAA CTT AAT-3'
A patient with xeroderma pigmentosum is prone to developing multiple skin cancers starting in
childhood. This occurs because of a mutation in a gene that codes for enzymes that help repair DNA
damage through the nucleotide excision repair (NER) pathways. How does the NER differ from other
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