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The PBRT book is excluded from this rule. If in doubt, get in touch with the course staff. Morgan Kaufmann, 2nd edition, July AK Peters, 2nd edition, August Instructions The assignments have to be solved and submitted individually. The final project will be done in groups. More information about the final project and the rendering competition will come later in the semester.

One notable example is the recently discovered replacement of lysine 27 with methionine in histone H3 or, more commonly, H3. In tumor cells carrying this oncohistone, trimethylation of lysine 27 on histone H3 H3K27me3 is strongly and globally depleted from chromatin 11 — H3K27me3 is a mark characteristic for facultative heterochromatin, and is associated with transcriptionally repressed regions H3K27 methylation is deposited, recognized and propagated by the Polycomb repressive complex 2 PRC2 , a multi-protein complex responsible for maintaining the silent state of the genes during development and cell differentiation 15 , PRC2-mediated H3K27me3 propagation is the result of dynamic interactions between the PRC2 complex and pre-existing H3K27me3, which allosterically activates PRC2 and facilitates the spreading of the mark to neighboring nucleosomes 17 — The observed depletion of H3K27me3 in H3.

Sequestration of PRC2 can explain how H3. However, retention of the mark in some genomic regions of mutant cells is inconsistent with the hypothesis that PRC2 is immobilized by H3. Regardless of the exact mechanism of PRC2 inhibition, several studies revealed H3.

Moreover, these studies have led to a detailed understanding of how H3K27 methylation states affect gene expression in tumor cells. However, several key aspects of how H3.

First, a precise understanding of how oncohistone incorporation remodels the H3K27me3 landscape genome-wide is lacking. Second, a causal link between the chromatin changes and the cancerous cell fate at a transcriptional level has not been established. And third, the cell-type specificity of H3. The available model systems to study consequences of the H3.

To overcome these limitations and to investigate these key outstanding questions, we introduced the H3. Mutant worms display ectopic DNA replication and cell-cycle progression in the germline.

We thus provide an animal model with a tumor-like phenotype induced by the oncohistone that does not require secondary mutations. Using this model system, we establish that PRC2 activity in mutant cells is affected both by H3. Moreover, we identify the JNK pathway as an important link between the global reorganization of heterochromatin and the replicative cell fate in both nematodes and human tumor-derived cell lines.

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Results H3. Worms carrying the H3. The mutant worms that do not show complete sterility have strongly reduced brood sizes. The mutation is semidominant, as sterility is also observed in heterozygous animals and can be induced by delivering extrachromosomal copies of H3.

In wild-type C. DNA replication is normally completely absent in proximal germ cells and only resumes during embryogenesis. Remarkably, in the H3. PDF guarantee certificate included can be used as proof of your barcode ownership. The barcode area is indicated in yellow on the template. Back-linking to www.

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