Download ANSWERS TO REVIEW QUESTIONS – CHAPTER 13

ANSWERS TO REVIEW QUESTIONS – CHAPTER 13
1. A eukaryotic cell can have several genomes? What are they? (p. 267, Figure 13.2)
Genomes—nuclear (can be more than one in allopolyploids)
—mitochondrial
—chloroplast
2.
Not all DNA in the genome encodes amino acid sequences of proteins. What roles, if any, do
other sequences play? (pp. 269–273)
The non-coding DNA in a genome can potentially have several functions. For instance, telomeres and
centromeres are involved in the maintenance of structural integrity, and other sequences may function
in chromosome pairing during meiosis. Still other sequences are required for the correct regulation of
gene expression, these include promoters 5' UTR elements and 3' UTR.
3.
DNA molecules in living cells are no longer thought to be inert molecules in terms of
possessing an unchanging DNA sequence. Why is this? (pp. 269–273)
A typical DNA sequence is not invariant, and many things can influence the DNA sequence of a
normal cell including the replication and relocation of transposons and programmed DNA
rearrangements such as those occurring in the immune system.
4. What is meant by the term ‘gene family’? (pp. 273–274)
A gene family is a group of sequence-related genes arising from duplication of a single ancestral gene.
5. What is the cause of variation in the DNA sequence? (pp. 276–278)
DNA variation (mutation) can be caused by agents such as UV light, nuclear radiation, chemical
mutagens, transposon insertion and DNA mismatch during replication.
6. How do mutations occur? (pp. 276–278)
Mutations are changes in the DNA sequence. They may be caused by mistakes during DNA replication
or through damage by radiation or chemicals. Mutations to a small number of base pairs are called
point mutations. A single base may be replaced with another (substitution), a base may be lost
(deletion) or a new base may be inserted (inserted). See Figure 12.9 for illustrations of various point
mutations. Major rearrangements of chromosomes in which sections of a chromosome are inverted or
transferred to another chromosome are also mutations.
Environmental agents such as radiation and some chemicals cause mutations. Some may remove bases
from the DNA backbone, so that bases are incorporated wrongly in the next round of replication.
Others mimic the structure of the four normal bases of DNA, but do not permit complementary pairing
and hence disrupt DNA replication. Other environmental mutagens bind with DNA to disrupt
replication.
7. How do cancer cells differ from normal cells? (pp. 279–284)
Cancer cells display unregulated cell division, non-differentiation and changed cell morphology to
allow invasive growth, and secrete enzymes to degrade the extracellular matrix.
8. How do dominant oncogenes and tumour suppressor genes differ? (pp. 280–284)
Dominant oncogenes are genes where a mutation of only a single allele is required for a cancerous
phenotype to develop. They can cause over-expression or aberrant expression of gene coding for
tumour formation. Tumour suppressor genes are genes where mutations cause loss of function that
usually results in tumour phenotype. Such genes are normally involved in cell cycle checkpoints.
9. What is the difference between a familial tumour and a sporadic tumour? (pp. 281–284)
Familial tumour—Genetic inheritance gives a predisposition for tumour formation.
Sporadic tumour—No inheritable trait is involved with tumour formation.
10. The retinoblastoma disease is inherited as a dominant genetic trait, yet both alleles of the
gene must be mutated for retinoblastoma to occur. What is the explanation for this? (p. 281)
Retinoblastoma is considered phenotypically as a dominant trait because individuals inheriting one
mutated allele will almost certainly undergo loss of function of the second allele at some stage, leading
to the disease state.