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1_WHAT ARE YOU PRINTING FOR DINNER

Q1: Methodological Application – Mapping 3D Genomic Architecture You are investigating a novel transcription factor (TF) and wish to distinguish its direct DNA binding sites from its indirect 3D contact sites (where it interacts with distant loci via looping). Based on the strategies described in the CUT&RUN research and Hi-C protocols, propose an experimental workflow using two distinct methodologies to map these interactions at near base-pair resolution. Why is traditional X-ChIP-seq insufficient for making this specific distinction?

Methodology (Denker & de Laat, 2017): Explain the difference between "one-to-all" (4C) and "all-to-all" (Hi-C) technologies. In what research scenario would you choose Capture-C over standard Hi-C?

Question 3: Logical Deduction of Epigenetic Tool Use Scenario: A hematologic malignancy is driven by the over-expression of the c-MYC oncogene. You are comparing two therapeutic strategies: using a BET inhibitor (an epigenetic reader tool) versus an EZH2 inhibitor (an epigenetic writer tool). Task: Based on their molecular mechanisms, deduce which tool would be more effective for immediate suppression of the MYC protein and explain why. Conversely, describe what would happen to the chromatin landscape if you used the writer inhibitor (EZH2i) on a system with H3K27me3-mediated repression.

Question 1: Experimental Application of DNA Methylation Mapping Scenario: You are investigating a novel candidate tumor suppressor gene, Gene-X, which you suspect is silenced in prostate cancer. You have access to patient tumor biopsies and matching normal tissue. Task: Describe an experimental approach using methylation-sensitive restriction enzymes (e.g., HpaII and MspI) to determine the methylation status of Gene-X’s promoter. Explain how you would interpret the resulting bands on a southern blot to confirm epigenetic silencing in the tumor versus the normal tissue.

Question 4: Genomic Integrity and Transgenerational Inheritance The lecturer describes how ddm1 mutants in Arabidopsis appear relatively normal in the first generation but show severe developmental defects by the fifth generation (F5). • Task: Explain the causal link between the loss of DDM1-mediated DNA methylation and the accumulation of physical DNA mutations across generations. • Logic Challenge: If you were to reintroduce a functional DDM1 gene into an F5 mutant line through crossing, would you expect the offspring to immediately return to a wild-type phenotype? Justify your answer by distinguishing between epimutations and transposon-induced DNA mutations