Identical twins are genetically identical at birth, but by age 50 they often show markedly different patterns of gene expression. What is the most plausible molecular explanation?
AAccumulated DNA mutations in one twin altered protein-coding sequences
BDivergent environmental exposures caused different DNA methylation and histone modification patterns to accumulate over time
COne twin's ribosomes became less efficient, reducing overall transcription rates
DMeiotic recombination events occurred in somatic cells, reshuffling gene order
Epigenetic marks — particularly DNA methylation and histone modifications — accumulate in response to environmental factors like diet, stress, and toxins, and are maintained through cell divisions. Identical twins share the same DNA sequence, so diverging gene expression reflects epigenetic, not genetic, differences. Option A is wrong because the question specifies expression patterns, not sequence changes; and large-scale somatic mutations or ribosome inefficiency do not explain the systematic, heritable differences observed.
Question 2 Multiple Choice
In a cell that has just undergone DNA replication, the newly synthesized strand lacks the methylation marks present on the original (template) strand. Which mechanism restores these marks?
ADe novo methyltransferases randomly methylate all cytosines on the new strand
BMaintenance methyltransferase (DNMT1) recognizes the half-methylated CpG sites and methylates the new strand to match the template
CRNA interference machinery detects unmethylated CpG sites and adds methyl groups
DThe cell does not restore methylation — daughter cells begin with blank epigenomes
DNMT1 is a maintenance methyltransferase that recognizes hemi-methylated CpG sites — where one strand is methylated and the newly synthesized strand is not — and methylates the new strand to match. This is the key mechanism by which epigenetic marks are faithfully propagated through cell division. De novo methyltransferases (DNMT3a/3b) establish new marks but do not maintain existing ones, and the cell absolutely does restore methylation patterns to preserve cell identity.
Question 3 True / False
Epigenetic modifications alter gene expression by changing the nucleotide sequence of DNA.
TTrue
FFalse
Answer: False
This is the central misconception about epigenetics. Epigenetic changes — DNA methylation, histone acetylation, histone methylation — modify how DNA is packaged and accessed without altering the underlying nucleotide sequence (A, T, G, C). The DNA sequence remains identical; what changes is whether and how that sequence is read. This is what makes epigenetics distinct from mutation.
Question 4 True / False
Most epigenetic marks in mammals are erased during gametogenesis, which is why true transgenerational epigenetic inheritance (marks passing from grandparent to grandchild) is the exception rather than the rule.
TTrue
FFalse
Answer: True
During gametogenesis (the formation of eggs and sperm), the genome undergoes extensive epigenetic reprogramming — most methylation marks are stripped and re-established. This prevents the faithful transmission of somatic epigenetic states across generations. Genuine transgenerational inheritance does occur in some cases (certain imprinted loci, for instance), but these are exceptions to a general pattern of epigenetic resetting, not the norm.
Question 5 Short Answer
A deletion in the chromosomal region 15q11-13 causes Prader-Willi syndrome when inherited from the father, but Angelman syndrome when inherited from the mother — even though the deleted region is the same. Why does the parent of origin matter?
Think about your answer, then reveal below.
Model answer: This is because of genomic imprinting. In the 15q11-13 region, different genes are imprinted (silenced) depending on which parental chromosome they're on. Some genes are only expressed from the paternal copy (the maternal copy is epigenetically silenced), while others are only expressed from the maternal copy. If the paternal copy is deleted, the maternally-imprinted genes have no functional copy — causing Prader-Willi. If the maternal copy is deleted, the paternally-imprinted genes lack a functional copy — causing Angelman. The same deletion has opposite consequences because epigenetic marks, not DNA sequence, determine which parental allele is active.
Imprinting means cells have already silenced one parental allele via methylation, so the remaining allele cannot compensate for a deletion on the other chromosome. This powerfully illustrates that epigenetic marks carry functional information beyond the DNA sequence — information that is parent-of-origin specific and established during gamete formation.