Lecture 10- Non-coding DNA evolution, transposable elements, endogenous viruses, and other mobile DNA Flashcards
what is the c-value paradox
uncertainty over why genome size (c value) and gene number don’t seem to correlate much
4 possible explanations for why non coding DNA exists
-has essential functions, such as regulation
-is just linked with functional genes
-has a structural function
-‘parasitic’- carried by genomes at their own expense
what features is genome size correlated with
nucleus size, duration of mitosis/meiosis, metabolic rate, plant seed size
what may explain these correlations other than causation
body/cell size as the third variable?
issue with nucleoskeletal function arguments
it has been found in some groups- nucleomorph algae- that nuclear size and DNA content don’t actually correlate
evidence for genome sizes being non-adaptive ‘junk’
simply not high enough effective pop size for junk to be removed from eukaryotic populations
not really any proper evidence of this idea once you correct numbers for common ancestry
satellite dna
100s of kb long highly repetitive tandem repeats, often in heterochromatin
minisattelite
moderately repetitive tandem repeats, with many VNTR loci
microsattelite
dispersed and either moderately or highly repetitive, 2-5bp repeats
what type of satellite has the highest mutation rate
microsatellite, 10ish mutations per gamete per generation
what is a transposable element
‘selfish’ dna elements which increase their copy number and jump around the genome
class I transposable element
retroelements which use an RNA intermediate, use/encode reverse transcriptase, e.g. LINEs (encode) and SINEs (use)
class II transposable elements
transposases and Ac-like elements- these are DNA elements and have terminal repeats at either side
another TE example
MITEs- rely on proteins they dont encode, made up of a few short repeats w terminal repeats
by how much can TE copy number increase in a single generation
20-100 copies
trait that can vary in different organisms which could help solve the c value paradox
different effectiveness of removal of TEs, e.g. drosophila seem to be better at it than mammals
impact of endogenous retroviruses on genomes
segmental duplication of genome, can become inserted into host genome
2 mechanisms of ERV host integration
co-option- host using viral genes for its own purposes, e.g. salivary amylase gene
recombination- viral genes can be involved in chromosomal recombination
what is ectopic exchange
crossing over of homologous dna sequences at non-allelic locations
how might levels of ectopic exchange be significant
may lead to pressure against TEs and recombination in general- some correlation between TE density and recomb rates in Drosophila and humans
how much of the (human) genome is estimated to be conserved and functional
5%, with 1.5% actually being genes
what are HARs
human accelerated regions, which are conserved in most mammals but diverge a lot in humans- e.g. HAR1 which is involved in cerebral cortex development
how much of the genome is functional according to ENCODE
80%, as 75% is transcribed and other parts are found in open chromatin, has TF binding sites etc- this implies function kinda
