Biomolecules I Flashcards
5’ cap is useful for
- removes exonuclease
- promotes ribosomal binding
- regulates nuclear export of mRNA
poly-A tail is useful for
- promotes translation
- regulates nuclear export
- termination of transcription
RNA editing: CDAR
-deamination of cytosine to uridine by cytosine deaminase
RNA editing: ADAR
-deamination of adenosine to inosine by hydrolytic deamination
microRNA (miRNA)
-gene silencing: miRNA binds to mRNA regions which are further prevented from translation or sent for degradation
Ribosomal RNA (rRNA)
-used for translation to make more ribosomes
Transfer RNAs (tRNAs)
-links codons in mRNA strands for corresponding AA for polypeptides
small nucleolar RNA (snoRNA)
-guide in covalent modifications of rRNA, tRNA, and snRNA through methylation and pseudouridylation (addition of an isomer of nucleotide uridine)
small nuclear RNA (snRNA)
- primary function is in processing of pre-mRNA in the nucleus
- formation of sRNP
How does spliceosome work?
- snRNA + snRNP
- removal of introns and ligating two exons together via trans-esterification reactions
How are proto-oncogenes converted into oncogenes?
- Deletion/point mutation: leads to a certain protein being overly expressed or is produced in normal amounts but is hyperactive.
- Gene amplification/increase in mRNA stability: prolongs the lifespan of mRNA which leads to more protein being over expressed
- Chromosomal rearrangement: translocation to a regulatory sequence which causes normal protein to be overly expressed
Cell cycle repressor proteins
represses genes that are essential for continuation of the cell cycle
two-hit hypothesis
In order for the mutation to manifest, both alleles must be defective (i.e. recessive alleles must be mutated to lead to cancerous phenotype)
Tumor suppressor gene: retinoblastoma protein (pRb)
- prevents the damaged DNA from replicating by preventing the progression of the cell cycle from G1 phase to S (synthesis) phase.
- attracts histone deacetylase (HDAC) which leads to repression of transcription
p53 protein
- Activates DNA repair protein when DNA has sustained damage
- stops cell cycle in G1 - S phase
- p53 binds to and activates several genes such as p21: which further binds to cyclin CDK complex that initiates the cell to move from G1 to S phase
- apoptosis
Two-hit hypothesis: dominant negative
-mutated p53 protein prevents the protein product of normal allele from functioning
where do mutations come from?
-spontaneous or inherited
Non-sense mutation
-genetic mutation that leads to a stop codon
Conservative mutation
-New AA is the same type as the original (from Glu to Asp: both are acidic)
Non-conservative mutation
-New AA is different type as the original (From Ser (polar) to Phe (non-polar))
point mutations
changes in the base pair substitutions (ACC ATC – ACT ATC)
Transition
substitution of purines by purines (A –> G; C –> T)
purines and pyrimidines
A – G (purines)
C – T (pyrimidines)