QUIZ 4

It allows cells to adapt to environmental changes and enables distinct activities of differentiated cell types in complex organisms.

At the level of transcription.

It catalyzes polymerization of ribonucleoside 5′-triphosphates (NTPs) in the 5′ to 3′ direction using a DNA template.

They disrupt the continuity of the DNA molecule.

Can occur naturally or due to ionizing radiation/chemicals.

It helps RNA polymerase identify the correct promoter sites for transcription initiation.

It is released, allowing the polymerase to continue elongation of the RNA strand.

The -10 (Pribnow box) and -35 sequences, which are recognized by σ factor for proper transcription initiation.

They facilitate DNA unwinding, making it easier for RNA polymerase to access the template strand.

A GC-rich inverted repeat sequence followed by 7 A residues, which forms a hairpin loop that causes RNA polymerase to dissociate.

They are involved in RNA splicing, transcript stability, and gene expression regulation.

Two α subunits, two β subunits, an ω subunit, and a σ factor (which stabilizes and helps identify promoters).

It binds to the -10 and -35 sequences, bends DNA (~90°), and unwinds about 10–14 bases to form an open-promoter complex.

It reads DNA in the 3′ to 5′ direction and writes RNA in the 5′ to 3′ direction.

The spacing (~24 nucleotides) allows the sigma factor to recognize both sequences without wrapping around DNA, aligning them correctly for RNA polymerase binding.

Eukaryotes have three RNA polymerases with unique promoters, more complex regulation, and additional processing steps like splicing and capping.

mRNA – Encodes proteins
rRNA – Forms ribosomes
tRNA – Transfers amino acids for protein synthesis
snoRNA – Modifies rRNA bases
miRNA/siRNA – Regulates transcript stability
piRNA – Regulates transposable elements
lncRNA – Controls chromatin accessibility (e.g., X inactivation)

RNA Pol I – Synthesizes rRNA
RNA Pol II – Synthesizes mRNA and some snRNA
RNA Pol III – Synthesizes tRNA, 5S rRNA, and other small RNAs

Chromatin architecture determines gene accessibility; heterochromatin (tight) represses transcription, while euchromatin (loose) allows transcription

They bind to complementary mRNA sequences to promote degradation or inhibit translation.

Proteins that bind to DNA sequences to either enhance or repress transcription by interacting with RNA polymerase and other regulatory proteins.What are the two major types of transcription termination in prokaryotes?

Intrinsic termination – Forms a hairpin loop in RNA, causing dissociation.
Rho-dependent termination – Uses Rho protein to release RNA from DNA.

The initial incorporation of nucleotides after open complex formation, which can lead to false starts before stable elongation begins.

Different sigma factors allow RNA polymerase to recognize specific promoters in response to environmental changes.

They reveal that RNA polymerase bends DNA at almost 90°, aiding in promoter recognition and strand separation.

The ribose nucleotide channel, which allows NTPs to enter and be polymerized in the active site.

The consensus sequences at -10 and -35 determine how well sigma binds, influencing transcription strength.

1. RNA polymerase and sigma bind to the promoter
2. DNA is bent and unwound (~10-14 bases)
3. Open complex forms, and nucleotides are added
4. Promoter clearance occurs, and sigma dissociates
5. RNA polymerase transcribes until it reaches the termination signal

GC-rich sequences form stable hairpins that cause RNA polymerase to stall and release RNA.

Mg²⁺ stabilizes the active site of RNA polymerase and helps catalyze the formation of phosphodiester bonds.

A process to rejoin broken strands using homologous DNA sequences.

Direct ligation of broken DNA ends.

Error-prone with a high frequency of mutations.

Uses a homologous sequence as a template for repair.

More accurate and error-free.

It facilitates genetic recombination through Holliday junction formation.

Genes encoding proteins for homologous recombination repair.

Mutations increase the risk of breast cancer.

They insert a less precise nucleotide opposite a lesion.

Regulated but can cause mutations if overused.

During active DNA processes like transcription or replication.

Lagging strand lesions do not slow replication significantly.

They can be repaired later.

Stalls replication as synthesis and unwinding occur simultaneously.

Pol epsilon disengages, and a translesion polymerase is recruited.

A "sloppier" translesion polymerase is used, introducing potential errors.

Used if translesion polymerase fails.

A new primase re-primes the lagging strand, leaving the lesion behind.

Uses a backup copy of DNA as a template for error-free repair.

Digest broken ends to create 3’ overhangs.

Strand invasion using intact homologous DNA.

DNA synthesis extends sequences beyond break points.

DNA ligation restores sequence continuity.

RPA prevents secondary structures in recombination.

Dmc1 facilitates strand invasion by testing sequence complementarity.

Intermediates formed during homologous recombination.

Cutting at different points determines genetic crossover.

Nucleotide excision repair.

Mutations increase the risk of skin cancer.

Creates targeted DNA breaks.

NHEJ repairs breaks but introduces sequence changes, effectively knocking out genes.