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02 Jun 2026, 08:43
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For much of the twentieth century, hereditary traits were understood to be transmitted exclusively through the nucleotide sequences in DNA. While environmental conditions massively impact each individual’s capability to reach genetic potential, it was generally thought impossible for those impacts to be heritable. Although this simplistic model has provided decades of enormous real-world productivity, recent evidence from the emerging field of epigenetics has revealed complications that researchers are only beginning to comprehend.
Epigenetic marks are chemical changes to DNA or associated structures that alter gene expression without changing the DNA’s nucleotide sequence. The two most studied mechanisms are DNA methylation, in which methyl groups attach to cytosine bases and silence nearby genes, and histone modification, in which chemical tags on the proteins around which DNA is wound loosen or tighten the helical shape of the DNA molecule itself, making genes more or less accessible to transcription machinery. Crucially, some of these marks are mitotically stable: they persist through cell division and thus can be transmitted into new cells—enabling the marks to persist longer than the cells’ regenerative cycle, which ranges from a few days for the epithelial cells lining the stomach up to decades for cells in the body’s largest bones.
The same quality also enables the transmission of epigenetic marks into sperm and egg cells, theoretically making possible the phenomenon of transgenerational epigenetic inheritance—the passing of epigenetic marks from parents on to their offspring through the reproductive process. Rodent studies have found altered gene expression patterns in the offspring of animals exposed to stressors such as toxins or nutrient deficiencies, even when the offspring have not been exposed to those stressors. In one well-known set of experiments, male mice fed a low-protein diet sired offspring with markedly altered hepatic gene expression, even though the offspring were raised on standard diets.
Skeptics caution that demonstrating true epigenetic inheritance requires ruling out alternative explanations, including behavioral transmission, microbiome transfer, and conventional genetic mutation. Whether such inheritance operates in humans remains altogether unknown, largely because the human genome has been shown to undergo extensive epigenetic reprogramming during the embryonic and early fetal stages—a process that would be expected to erase most parental marks.
The passage implies that epigenetic reprogramming of the human genome during the embryonic and early fetal stages is relevant to the debate over transgenerational inheritance because it
A. cannot possibly co-occur in the same individual as transgenerational epigenetic inheritance
B. confirms the presence of transgenerational epigenetic inheritance in human beings
C. narrows the range of possible mechanisms of epigenetic modification to human genes
D. raises the possibility that transgenerational epigenetic inheritance may be active in cases where it leaves no lasting evidence
E. suggests that human genes are more amenable than rodent genes to epigenetic modification than that of rodents
Epigenetic marks are chemical changes to DNA or associated structures that alter gene expression without changing the DNA’s nucleotide sequence. The two most studied mechanisms are DNA methylation, in which methyl groups attach to cytosine bases and silence nearby genes, and histone modification, in which chemical tags on the proteins around which DNA is wound loosen or tighten the helical shape of the DNA molecule itself, making genes more or less accessible to transcription machinery. Crucially, some of these marks are mitotically stable: they persist through cell division and thus can be transmitted into new cells—enabling the marks to persist longer than the cells’ regenerative cycle, which ranges from a few days for the epithelial cells lining the stomach up to decades for cells in the body’s largest bones.
The same quality also enables the transmission of epigenetic marks into sperm and egg cells, theoretically making possible the phenomenon of transgenerational epigenetic inheritance—the passing of epigenetic marks from parents on to their offspring through the reproductive process. Rodent studies have found altered gene expression patterns in the offspring of animals exposed to stressors such as toxins or nutrient deficiencies, even when the offspring have not been exposed to those stressors. In one well-known set of experiments, male mice fed a low-protein diet sired offspring with markedly altered hepatic gene expression, even though the offspring were raised on standard diets.
Skeptics caution that demonstrating true epigenetic inheritance requires ruling out alternative explanations, including behavioral transmission, microbiome transfer, and conventional genetic mutation. Whether such inheritance operates in humans remains altogether unknown, largely because the human genome has been shown to undergo extensive epigenetic reprogramming during the embryonic and early fetal stages—a process that would be expected to erase most parental marks.
The passage implies that epigenetic reprogramming of the human genome during the embryonic and early fetal stages is relevant to the debate over transgenerational inheritance because it
A. cannot possibly co-occur in the same individual as transgenerational epigenetic inheritance
B. confirms the presence of transgenerational epigenetic inheritance in human beings
C. narrows the range of possible mechanisms of epigenetic modification to human genes
D. raises the possibility that transgenerational epigenetic inheritance may be active in cases where it leaves no lasting evidence
E. suggests that human genes are more amenable than rodent genes to epigenetic modification than that of rodents
02 Jun 2026, 08:43
Kudos
Bookmarks
Official Solution:
For much of the twentieth century, hereditary traits were understood to be transmitted exclusively through the nucleotide sequences in DNA. While environmental conditions massively impact each individual’s capability to reach genetic potential, it was generally thought impossible for those impacts to be heritable. Although this simplistic model has provided decades of enormous real-world productivity, recent evidence from the emerging field of epigenetics has revealed complications that researchers are only beginning to comprehend.
Epigenetic marks are chemical changes to DNA or associated structures that alter gene expression without changing the DNA’s nucleotide sequence. The two most studied mechanisms are DNA methylation, in which methyl groups attach to cytosine bases and silence nearby genes, and histone modification, in which chemical tags on the proteins around which DNA is wound loosen or tighten the helical shape of the DNA molecule itself, making genes more or less accessible to transcription machinery. Crucially, some of these marks are mitotically stable: they persist through cell division and thus can be transmitted into new cells—enabling the marks to persist longer than the cells’ regenerative cycle, which ranges from a few days for the epithelial cells lining the stomach up to decades for cells in the body’s largest bones.
The same quality also enables the transmission of epigenetic marks into sperm and egg cells, theoretically making possible the phenomenon of transgenerational epigenetic inheritance—the passing of epigenetic marks from parents on to their offspring through the reproductive process. Rodent studies have found altered gene expression patterns in the offspring of animals exposed to stressors such as toxins or nutrient deficiencies, even when the offspring have not been exposed to those stressors. In one well-known set of experiments, male mice fed a low-protein diet sired offspring with markedly altered hepatic gene expression, even though the offspring were raised on standard diets.
Skeptics caution that demonstrating true epigenetic inheritance requires ruling out alternative explanations, including behavioral transmission, microbiome transfer, and conventional genetic mutation. Whether such inheritance operates in humans remains altogether unknown, largely because the human genome has been shown to undergo extensive epigenetic reprogramming during the embryonic and early fetal stages—a process that would be expected to erase most parental marks.
The passage implies that epigenetic reprogramming of the human genome during the embryonic and early fetal stages is relevant to the debate over transgenerational inheritance because it
A. cannot possibly co-occur in the same individual as transgenerational epigenetic inheritance
B. confirms the presence of transgenerational epigenetic inheritance in human beings
C. narrows the range of possible mechanisms of epigenetic modification to human genes
D. raises the possibility that transgenerational epigenetic inheritance may be active in cases where it leaves no lasting evidence
E. suggests that human genes are more amenable than rodent genes to epigenetic modification than that of rodents
Epigenetic reprogramming in human embryos is mentioned at the very end of the passage. The main significance of this phenomenon is laid out immediately after the author’s description of the phenomenon itself, in the modifier linked with a dash: “a process that wolud be expected to erase most parental marks”. In other words, IF indeed there is any passing down of epigenetic marks from human parents to their children, this “reprogramming” process will overwrite the majority of those marks very early in a baby’s gestation, leaving no evidence of the marks having been passed down in the first place. Choice D properly summarizes this stated significance.
INCORRECT ANSWERS:
(A) A process can only overwrite the results of another process if both of those processes DO co-occur, so the cases of epigenetic reprogramming in which the author is interested all directly contradict choice A.
(B) Quite the opposite: The reprogramming process, by overwriting the results of epigenetic inheritance, will make it much more difficult to confirm that any such inheritance has occurred even in cases where it actually has.
(C) The text contains nothing to suggest that the fetal epigenetic reprogramming process can narrow down the set of potential mechanisms for epigenetic marking. If anything, the reprogramming process—which destroys most evidence of whatever epigenetic marks may have been inherited—may even expand that set of potential mechanisms, by destroying evidence that would have narrowed it!
(E) The author does not consider any probabilities of ocurrence for epigenetic modifications let alone compare those probabilities across species.
Answer: D
For much of the twentieth century, hereditary traits were understood to be transmitted exclusively through the nucleotide sequences in DNA. While environmental conditions massively impact each individual’s capability to reach genetic potential, it was generally thought impossible for those impacts to be heritable. Although this simplistic model has provided decades of enormous real-world productivity, recent evidence from the emerging field of epigenetics has revealed complications that researchers are only beginning to comprehend.
Epigenetic marks are chemical changes to DNA or associated structures that alter gene expression without changing the DNA’s nucleotide sequence. The two most studied mechanisms are DNA methylation, in which methyl groups attach to cytosine bases and silence nearby genes, and histone modification, in which chemical tags on the proteins around which DNA is wound loosen or tighten the helical shape of the DNA molecule itself, making genes more or less accessible to transcription machinery. Crucially, some of these marks are mitotically stable: they persist through cell division and thus can be transmitted into new cells—enabling the marks to persist longer than the cells’ regenerative cycle, which ranges from a few days for the epithelial cells lining the stomach up to decades for cells in the body’s largest bones.
The same quality also enables the transmission of epigenetic marks into sperm and egg cells, theoretically making possible the phenomenon of transgenerational epigenetic inheritance—the passing of epigenetic marks from parents on to their offspring through the reproductive process. Rodent studies have found altered gene expression patterns in the offspring of animals exposed to stressors such as toxins or nutrient deficiencies, even when the offspring have not been exposed to those stressors. In one well-known set of experiments, male mice fed a low-protein diet sired offspring with markedly altered hepatic gene expression, even though the offspring were raised on standard diets.
Skeptics caution that demonstrating true epigenetic inheritance requires ruling out alternative explanations, including behavioral transmission, microbiome transfer, and conventional genetic mutation. Whether such inheritance operates in humans remains altogether unknown, largely because the human genome has been shown to undergo extensive epigenetic reprogramming during the embryonic and early fetal stages—a process that would be expected to erase most parental marks.
The passage implies that epigenetic reprogramming of the human genome during the embryonic and early fetal stages is relevant to the debate over transgenerational inheritance because it
A. cannot possibly co-occur in the same individual as transgenerational epigenetic inheritance
B. confirms the presence of transgenerational epigenetic inheritance in human beings
C. narrows the range of possible mechanisms of epigenetic modification to human genes
D. raises the possibility that transgenerational epigenetic inheritance may be active in cases where it leaves no lasting evidence
E. suggests that human genes are more amenable than rodent genes to epigenetic modification than that of rodents
Epigenetic reprogramming in human embryos is mentioned at the very end of the passage. The main significance of this phenomenon is laid out immediately after the author’s description of the phenomenon itself, in the modifier linked with a dash: “a process that wolud be expected to erase most parental marks”. In other words, IF indeed there is any passing down of epigenetic marks from human parents to their children, this “reprogramming” process will overwrite the majority of those marks very early in a baby’s gestation, leaving no evidence of the marks having been passed down in the first place. Choice D properly summarizes this stated significance.
INCORRECT ANSWERS:
(A) A process can only overwrite the results of another process if both of those processes DO co-occur, so the cases of epigenetic reprogramming in which the author is interested all directly contradict choice A.
(B) Quite the opposite: The reprogramming process, by overwriting the results of epigenetic inheritance, will make it much more difficult to confirm that any such inheritance has occurred even in cases where it actually has.
(C) The text contains nothing to suggest that the fetal epigenetic reprogramming process can narrow down the set of potential mechanisms for epigenetic marking. If anything, the reprogramming process—which destroys most evidence of whatever epigenetic marks may have been inherited—may even expand that set of potential mechanisms, by destroying evidence that would have narrowed it!
(E) The author does not consider any probabilities of ocurrence for epigenetic modifications let alone compare those probabilities across species.
Answer: D
