Section 8
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What are LADs, NADs, and TADs?
• LADs: Lamina-associated domains • NADs: Nucleolus-associated domains • TADs: Topologically associated domains TADs are looped domains where regions interact frequently within but rarely with others, while LADs and NADs are associated with transcriptionally inactive heterochromatin.
What is the role of CTCF and cohesin in TADs?
They form the boundaries of TADs CTCF and cohesin are architectural proteins that regulate genome organization.
True or false: Heterochromatin is localized to the nuclear lamina by binding to lamins and the lamin B receptor.
TRUE This localization is characteristic of transcriptionally inactive heterochromatin.
What percentage of the human genome is made up of LADs?
~40% LADs are associated with transcriptionally inactive heterochromatin at the nuclear periphery.
What are NADs and how do they relate to LADs?
• NADs: Nucleolus-associated domains • Overlap with LADs NADs are associated with the nucleolus and contain DNA sequences similar to those in LADs.
What is the basic definition of a tumor?
Any abnormal proliferation of cells Tumors can be benign (localized) or malignant (invading and metastasizing).
What distinguishes benign tumors from malignant tumors?
• Benign: Remain localized • Malignant: Invade and metastasize Only malignant tumors are referred to as cancers.
What are proto-oncogenes?
Normal cell genes that regulate cell proliferation They can become oncogenes when mutated or abnormally expressed.
How do oncogenes differ from proto-oncogenes?
• Oncogenes: Abnormally expressed or mutated forms • Proto-oncogenes: Normal regulatory genes Oncogenes induce abnormal cell proliferation and tumor development.
What is density-dependent inhibition in normal cells?
Normal cells cease proliferation upon reaching a finite cell density Cancer cells do not respond to this inhibition and continue to proliferate.
What type of carcinogen is asbestos?
Chemical carcinogen It acts by inducing mutations in cellular genes.
What is the impact of recombination of viral DNA with raf?
Leads to fusion proteins that may lose regulatory domains This can generate oncogene proteins with altered activity.
What are fusion proteins in the context of oncogenes?
Proteins expressed as a result of the combination of oncogenes with viral sequences Many oncogenes, such as raf, are expressed as fusion proteins with viral sequences at the amino terminus.
How do recombination events contribute to oncogene formation?
They lead to the generation of fusion proteins by capturing proto-oncogenes This often occurs during the capture of proto-oncogenes by retroviruses.
What is the consequence of deletions during the formation of fusion proteins?
Loss of regulatory domains controlling proto-oncogene activity This can generate oncogene proteins that function in an unregulated, hyperactive manner.
What critical sequences are deleted in the viral raf oncogene?
Amino-terminal sequences of the normal Raf protein These sequences are essential for the normal regulation of Raf protein kinase activity.
What is the result of the deletion of the amino-terminal sequences in the raf oncogene?
Unregulated (constitutive) activity of the oncogene-encoded Raf protein This hyperactivity drives abnormal cell proliferation, resulting in transformation.
What are the two domains of the Raf proto-oncogene protein?
• Amino-terminal regulatory domain • Carboxy-terminal protein kinase domain In the viral Raf oncogene protein, the regulatory domain is deleted and replaced by partially deleted viral Gag sequences.
What happens to the Raf kinase domain in the viral Raf oncogene?
It becomes constitutively active This causes cell transformation.
How do point mutations affect oncogenes?
They result in single-amino-acid substitutions in the oncogene products Such substitutions can lead to unregulated activity of the oncogene proteins.
What is an important example of point mutations in oncogenes?
ras oncogenes These are discussed in terms of their role in human cancers.