Chapter 19 Flashcards
epigenetics
study of the change in organisms caused by the modification of gene expression
AHMED
Acetylation of Histones
Methylation of DNA
Increased methylation of DNA
methyl groups inhibit transcription by changing the shape and condensing DNA and making DNA not inaccessible to transcription factors
Increased acetylation of histones
addition of acetyl groups to the histone proteins associated with DNA in the nucleus of cells. This reduces the affinity between the histones and DNA, leading to a more relaxed chromatin structure, increasing the accessibility for transcription factors
movement of transcription factors
moves from the cytoplasm into the nucleus to stimulate or inhibit transcription of target genes
what do transcription factors do
bind to a specific region of DNA and regulates transcription
oestrogen’s role as a transcription factor
binds to a complementary receptor on a transcription factor, activating it. This alters the shape and releases an inhibitor molecule from the DNA binding site on the transcription factor. The transcription factor can then move into the nucleus via the nuclear pores and bind with DNA initiating particular genes
RNA interference
•Enzyme cuts a large double stranded section of RNA into siRNA
• siRNA will bind with certain proteins (RISC proteins) forming a complex.
• The siNA will lose/unwind one of its strands (becoming single stranded).
• siNA guides an enzyme to the mRNA molecule and binds by complementary base pairing.
•If there is exact complementary binding then the mRNA will be degraded.
• If binding is partly complementary, mRNA is not degraded but siRNA remains bound and stops translation from occurring.
• Both effects result in the non-translation of the mRNA molecule to polypeptide.
application of genome projects
identifying potential antigens for use in vaccine production
6 types of mutations
addition, deletion, substitution, inversion, duplication, translocation
3 types of stem cells
totipotent, pluripotent, multipotent
proto-oncogenes
stimulate normal cell division
oncogenes
are mutated proto-oncogenes which cause tumour growth
how do oncogenes cause cancer
code for a growth factor which is produced in excess. This growth factor permanently activates cell surface membrane receptors which stimulate cell division
TSGs
if mutated, tumour suppressor genes can no longer inhibit cell division. As a result the cell may die or could divide to form a tumour.
Abnormal methylation of TSGs is also associated with tumour formation as methylation prevents TSGs from being activated but activates oncogenes and forms tumours
