11. Edge colouring of graphs, Xe(G) and its relation to A(G). Vizing's theorem (without proof), Shannon's theorem (without proof), Konig's theorem about the edge chromatic number of bipartite graphs.

18- Citología - Núcleo: Estructura y Cromatina

Bipartite graphs: definition, relationship with odd cycles. Vertex coloring: proper col- oring, chromatic number x(G) (!!!), relationship to clique number w(G) and maximum degree A(G). Greedy coloring algorithm and its bound.

Cell Biology: Chromatin and Cell Cycle Regulation

Bone homeostasts: bone REmodeling

6.7 Bone Remodelling

6.6 Bone Remodeling

Chromatin and DNA Packing

Chromatic Chords

Bone Remodeling and Repair

Chromatic Mediants

Nucleic Acids and Chromatin

Eukaryotic Transcription and Chromatin Structure

Q4: Logical Deduction – Chromatin Remodeling and CHD2 Pathology A patient is identified with a de novo mutation that specifically disables the SNF2-like ATPase domain of the CHD2 protein while leaving its tandem chromodomains intact. Based on the biochemical roles of CHD subfamilies, deduce how this mutation alters nucleosome maturation and spacing. Contrast this with a hypothetical mutation that instead disables the chromodomains; which defect would more severely impair the protein’s ability to "recognize" the H3K4me2/3 active chromatin mark?

Therapeuticspeculation: Discuss how forced chromatin looping could be used as a precision medicine approach for patients with -thalassaemia

3D Organization: Define the "extrusion model" for chromatin loop formation. Explain how the orientation of CTCF binding sites (convergent vs. divergent) acts as a "roadblock" for cohesin in this model

Question 4: Applying Methodology to Chromatin Boundaries Scenario: A researcher uses ChIP-seq to map the distribution of H3K4me3 (an activating mark) and H3K27me3 (a repressive mark) at a specific locus in both Embryonic Stem (ES) cells and advanced Cancer cells. Task: 1. Predict the distribution of these marks in the ES cells, referencing the concept of a "bivalent state". 2. Describe how this ChIP-seq profile would change in a cancer cell undergoing "epigenetic switching". 3. Logically deduce how a breakdown in CTCF insulator function would impact these ChIP-seq boundaries

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 2: Causal Relationships in Vernalization In the vernalization response of Arabidopsis, the FLC (FLOWERING LOCUS C) gene is epigenetically silenced to allow flowering. • Task: Explain the causal relationship between the H3K27me3 histone mark and the chromatin state of the FLC locus during and after winter. • Logic Challenge: Based on the molecular players described (e.g., the PRC2 complex), predict what would happen to the plant's flowering behavior if it possessed a "writer" mutation that prevented the deposition of H3K27me3 marks even when exposed to cold.

Human Bone Growth, Structure, and Remodeling: A Comprehensive Quizlet