RNA Editing and Genetic Relatedness Quiz

Study Notes

LDL receptor gene exons are closely related to C9 complement gene exons and EGF-precursor gene exons.
RNA editing involves targeted modifications of mRNA sequences to alter coding information.
Mechanisms include site-specific deamination and guide RNA directed insertion or deletion of uridines.

Targeted deamination can convert cytosine (C) in mRNA to uracil (U); notably, cytidine deaminase acts on apolipoprotein B mRNA.
This conversion results in a stop codon (UAA) in intestinal cells, leading to truncated proteins, while liver cells produce full-length proteins.
APOBEC3G (A3G) cytidine deaminase targets HIV cDNA, converting C to U, which damages the viral genome.
HIV exploits the Vif protein to degrade A3G, thus protecting itself from the host's antiviral mechanism.
Adenosine deaminase acting on RNA (ADAR) converts adenine (A) to inosine (I); this editing is crucial for mRNA coding ion channels in mammalian brains, with failure resulting in brain development issues.

Guide RNAs found in trypanosome mitochondria facilitate U addition or deletion, altering reading frames according to specific patterns dictated by their sequences.
U insertion processes involve endonuclease cutting mRNA opposite guide RNA loops, allowing uridines to be inserted and gaps to be sealed by ligase.

Fully processed mRNA (capped, spliced, and polyadenylated) is selectively transported to the cytoplasm.
The export process is tightly regulated, distinguishing mature mRNA from damaged or misprocessed RNAs and liberated introns.
Identification of mRNA for export relies on specific proteins, including Poly-A binding proteins, SR proteins, and exon-exon junction proteins.

Eukaryotic genes feature original pre-mRNA transcripts with introns (non-coding) and exons (coding), necessitating precise splicing.
Drosophila Dscam gene, comprising 24 exons, enables the production of 38,016 protein isoforms, crucial for neural patterning and immunity.
The mutually exclusive splicing of exon 6 is regulated via an intron docking site interacting with selector sequences for different exon 6 variants.
Only one variant can bind to the docking site at a time, while splicing repressor protein prevents the inclusion of other exons.

Splicing enhancers and silencers influence nearby splice sites by binding splicing activators and repressors, adapting splicing machinery to varying conditions.
Silencer mechanisms help direct splicing decisions, impacting the generation of alternative mRNA isoforms.