gene organisation, transcription and regulation

Question 1

c-value paradox

Answer 1

complexity of genome not necessarily related to genome size; genome is constant in all cells of species

Question 2

non-coding RNA

Answer 2

any RNA not translated into protein; include tRNA, rRNA and snRNA, and regulatory ncRNA

Question 3

microRNA use

Answer 3

translation

Question 4

siRNA/RNAi use

Answer 4

viral defence

Question 5

piRNA use

Answer 5

germ cell production

Question 6

long ncRNA use

Answer 6

X-inactivation (lyonisation): one X-chromosome in females inactivated by being silenced in transcriptionally inactive heterochromatin; prevents females having twice as many X genes as men; random chance of lysation; remains inactive in all derivatives

Question 7

using RNAi as viral defence to slice mRNA

Answer 7

antisense RNA hybridises with mRNA with strong complementary attraction to blocks translation (as forms dsRNA); dicer (essential for no defects) breaks up dsRNA into smaller fragments; RNAi-endonuclease activity removes one RNAi stand (“passenger”), requiring “Argonaut-piwi” proteins (retained strand is antisense to target strand); RISC forms which recognises and cleaves target mRNA molecules with complementary sequence to RNAi, forming sliced mRNA

Question 8

miRNA use

Answer 8

double stranded; involved in gene regulation by blocking translation

Question 9

production of miRNA

Answer 9

transcribed in nucleus into long primary pri-miRNA by RNA pol II and III; processed by Drosha and exported to cytoplasm as pre-miRNA; passed into RISC complex (some sequences become RNAi); once become miRNA, target genes at RNA level and silence them (“gene knockdown”)

Question 10

miRNA base pairing

Answer 10

incompletely complementary to target mRNAs: “seed”; mismatch → bulge → 3’ region complementary

Question 11

miRNAs in human disease (CLL)

Answer 11

deletion in gene loses miRNA; promotes CLL; supplementing miRNA removes CLL