Genetic Parasites

Question 1

What is a genetic pararite?

Answer 1

Parasite of genetic system, cheats the reproductive system

Question 2

What is Mendelian inheritance?

Answer 2

On average half offspring receive one allele and half the other allele - gives stable allele frequencies

Question 3

What is meiotic drive/genetic drive?

Answer 3

If an allele is inherited by more than half the parent’s offspring
Allele will increase in frequency
These are parasites on the rest of the genome, need not increase organism’s fitness, only its own

Question 4

How do you model meiotic drive?

Answer 4

If Bb heterozygotes made extra proportion (+r/2) B allele, and (-r/2) b allele, then B becomes more common
For parents that are heterozygote this affects offspring frequencies
P’B = PB + 1/2rPBb

Question 5

How does a driving allele spread?

Answer 5

Spreads as though it confers a fitness advantage to host

Even if it reduces overall fitness will still spread as long as reduction is fitness is less than advantage of drive

Question 6

What are killer alleles?

Answer 6

Any allele that can kill or damage the gametes containing other allele it will spread
One hypothetical mechanism = poison-antidote system
If B makes slow long-lasting poison and short lived antidote
Another mechanism is for a product of B to directly target sequence of b

Question 7

What is over-replication?

Answer 7

Any locus that can copy itself around the genome will spread

Question 8

What is allelic conversion?

Answer 8

Any allele that can replace the other allele with itself will spread

Question 9

What is biased segregation?

Answer 9

Any allele that can ensure it ends up in the cell lineage leading to the egg will spread
B chromosomes do this by ensuring asymmetric division in the germline so they are biased toward ending up in the gametes

Question 10

How does drive select for suppressors?

Answer 10

If genetic parasites decrease fitness of host it selects for suppressor alleles in 2 ways:

1. If B allele has biased transmission it spreads at expense of b allele, any new variant b’ that can stop B will have advantage over b
2. If driving B allele reduces overall fitness then any allele G (at any other locus in genome) that can stop B will have advantage over g

Question 11

What is the t-haplotype in mice?

Answer 11

Works through sperm so only impacts males
Homozygote WT males (+,+) produce WT sperm
Heterozygote males for t (+,t) WT sperm poor quality compared to t-haplotype
Homozygote t-haplotype males (t,t) always sterile
Will never spread to fixation

Question 12

What are the genetics of the t-haplotype?

Answer 12

Version of chromosome 17, suppressed recombination due to overlapping inversions

Question 13

How does the t-haplotype spread?

Answer 13

Poison-antidote system
Distorter loci are expressed in all sperm from heterozygotes, these hyper activate Smok1 and impede sperm motility
In t-haplotype sperm this is reduced by dominant-negative action of Tcr

Question 14

What are transposable elements?

Answer 14

Element that can copy itself around the genome

Arguably the most dominant parasite

Question 15

What are the 2 types of transposable element?

Answer 15

DNA ‘cut & paste’ elements - excise themselves from genome and insert elsewhere using transposase encoded themselves: repair using sister chromatid or jumping in front of replication fork
Include Mariner and P-elements

RNA ‘copy & paste’ retrotransposons - expressed as RNA and reverse-transcribe into genome with reverse-transcriptase encoded themselves
Include LINES and Copia

Question 16

How have P-elements spread in Drosophila?

Answer 16

Spread from D. willistoni to D. melanogaster between 1950-1970
Spread to D. simulans around 2004

Question 17

How much of the human genome is TE?

Answer 17

~45% genome TEs, mostly Alu and L1 LINE elements

Question 18

Why are TEs damaging?

Answer 18

Transposition into/near genes can cause genetic diseases
Ectopic recombination causes loss and rearrangement of large parts of genome - can cause lethal mutations/cancer
Uncontrolled transposition in germline can cause so much damage that apoptosis leads to infertility

Question 19

What is the evidence that TEs are deleterious?

Answer 19

Deleterious alleles kept rare by selection
TE insertions tend to be rarer than would be predicted for neutral mutations
They are deleterious (selected against)

Question 20

How are TEs suppressed?

Answer 20

The piRNA pathway of animals directs suppression of TEs in germline by using small-RNA guides to target repressive chromatin marks to transcribed TEs in the germline
When this pathway is knocked out there’s increased TE expression

Question 21

What are cytoplasmic endosymbionts?

Answer 21

Cytoplasmic genomes (mitochondria/chloroplasts) don’t display Mendelian inheritance, but can cheat

Question 22

How can bacteria skew sex ratios?

Answer 22

Cytoplasmic endosymbionts are inherited maternally through the cytoplasm
They can ‘cheat’ by ensuring host has more female offspring

Can kill males but doesn’t increase frequency, only proportion
So females have to do better, and can do this by eating eggs of dead males or have more space on plant so are bigger

Can become feminiser and turn all offspring into females

Question 23

How does the mechanism of male-killing work?

Answer 23

Eg. in flies S. poulsonii
Deletion in 1065AA protein with ankyrin repeats and de-ubiquitinase domain
Requires expression of Male-Specific Lethal (MSL) a fly gene that mediates dosage compensation in males - their X chromosomes need to express twice as much as X chromosomes in females