A. Describe one limitation of the study that you noticed, or a question that you think remains unanswered after reading the paper. (2–4 sentences.)

B. Propose one realistic follow-up experiment that could be done in a lab to address that limitation or question.

• What would you measure (for example, a particular epigenetic mark, gene expression level, or phenotype)?
• How would the result help strengthen or challenge the authors’ conclusions?

Choose one main figure (not a cartoon model) that shows epigenetic data.

A. Write the figure number

 (e.g.,

Fig. 2). In 3–4 sentences, explain:

• What comparison is being made?

  (e.g., control vs. treatment, wild-type vs. mutant, etc.)

• What epigenetic readout

   is

  shown (for example, ChIP-seq signal, ATAC-seq peaks, DNA methylation

  percentage, etc.)?

B. Pick one panel

 from

that figure (e.g., Fig. 2B) and answer:

• What does a higher

   signal/peak/value

  mean biologically in that panel?

• What is the 

  main

  conclusion

   the authors draw from this panel?

Please attach a screenshot of the figure chosen.

Pick one technique used in the paper that measures an epigenetic feature (for example, ChIP-qPCR, ChIP-seq, ATAC-seq, bisulfite sequencing, CUT&RUN, etc.).

A. Name the technique and, in simple terms, explain what it measures.

B. Based on a result in the paper using this technique, give:

• One thing the authors can safely conclude about gene regulation or chromatin state.
• One thing they cannot conclude from this technique alone (for example, they might see correlation but not prove cause-and-effect).

A. In your own words, describe the main biological question of the paper and how epigenetic regulation is involved.

B. Name one specific epigenetic mark or mechanism in the paper that we have discussed in class, and explain very simply how the authors think it affects gene expression in this system. 

Use your class notes (not the internet) for this question.

A. Think of one example from a lecture or another paper we discussed in part III of class where the same epigenetic regulatory pathway played a role (e.g., X inactivation, addiction, metabolism and diet, learning and memory, etc.). Briefly describe that example.

B. Compare your chosen exam article to that class example by answering:

• One similarity is in how epigenetic marks affect gene expression.
• One difference in either the type of epigenetic mark, or the biological process being regulated (development, disease, plasticity, etc.).

Please, identify the research articles that we discussed in class

(vignettes # 1 – 15), you chose to answer this exam (first author, year): 

There are four main levels of chromatin compaction: Please describe the structure of chromatin at the level of compaction referred to as "beads-on-a-string" and indicate its effect on transcription.

Explain the difference between Active and Passive demethylation of DNA?

Regarding the histone code, what is the main difference between histone methylation and histone acetylation?

Explain the advantage of having multiple different core-promoter elements regulating a single gene.