Download Evolution Advanced Levels of Selection Where does evolution act

Evolution Advanced
Levels of Selection
Where does evolution act? Gene/cell/mitochondria/individual?
Frogs, many eggs/wolves in groups  wrong arguments! Optimal for the individual, many traits
unvorteilhaft for level of species
Selfish gene perspective
There are replicators. Those need and build vehicles (=interactors). Replicators are basically
information, which is always coded in DNA. Examples for replicators are the germ line replicators or
the "dead" replicators. Dead ones don't replicate, like skin cells, they don't have "children". Why did
they agree to be dead? Because they are highly related to germ line replicators. Nature can not pick
genes, it can only pick the vehicles!
b = fitness benefit for recipient; r = relatedness; c = fitness cost for helper
"cooperation is more likely to evolve between highly related vehicles" -> eukaryotes are a product of
a shift from prokaryotes = fusion between lower-level-vehicles
Forces
Repulsive: resource competition
Attractive: inclusive fitness (relatedness!), large size (predation!)
Centrifugal: solitary existence
Dictyostelium discoideum -> "slug" with stalk
Meiotic Drive -> mouse t/+
Genes in the t-complex produce a toxic effect on + sperm. The genes in the t-complex are immune
due to a produced antidote. t/+ mice produce to 90-100% t-carrying sperms. The t/t combination is
lethal, caues male-sterile or reduced viability. However, the + is speaking of individual level favoured!
-> stable coexistence of t and +
Male-sperm conflict: sperm are in concurrence to each other, this is bad for individual!
Conditions for group selection: 1) groups need to have high risk of extinction 2) migration rate
between groups need to be low
Evolution of Individuality
p2 + 2pq + q2 = 1
p+q=1
[p -> A]
Fundamental constraint: to divide AND retain motility at the SAME time, a cell needs:
 Microtubule organising centers that can perform both tasks simultaneously
 Multiple microtubule organising centers
Solution: nuclear division without spindel apparatus! Others haven't solved it, have to
withdraw flagellates
Next problem: What does an embryo do? Gastrulation! Inner cells -> dividing, outer cells ->
motility
Two fundamental problems:
1. how is competition between cell lineages avoided?
2. which cell lineage gives rise to the next generation?
Discussion:
1. Scenario of a mutation -> outgrow the other (older) cells in the embryo, but: it must be in
interest of whole cell! Individual selection is required to counteract selfish gene lineages. It
must recognise cheaters in own cells. Self-/foreign-recognition system!
2. "Agreement" to best candidate of common ancestor. Solution: soma vs. Germ line
distinction -> Differenzierung!
Hardy-Weinberg-equilibrium
Soma vs. Germ line distinction:
somatic cells can increase their fitness by collaboration! Just possible because of common
goal (see bee's queen), some somatic cells are available for risky jobs -> apoptosis. Division
of labour, cellular differentation. Transition for uni- to multicellularity in about 75% of all
protist group, generally all cells remain totipotent! But strict soma/germ line distinction rare.
Drosophila -> first 13 rounds of division maternal control! So she decides cell determination.
Hydra viridis: I-Zellen -> Gameten/Soma; aus Soma -> I-Zellen
Individuality:
Is only an approximation in most cases! -> what "helps":
Passage through a single cell stage/soma vs germ line distinction/the larger and more
complex -> then dependence on individuality!
Risk of cheating: accessing the germ line later in development/by refusing to refrain from
division -> cancer!
Botryllus schlosseri: asexual buddying -> colony -> common exhalant siphon, common blood
vessel -> contact unrelated/related/self colonies-> fusion with those who share at least one
allel -> chimeric individuals! One colony is reproductively dead!
Evolution of development
Life cycle = repeated sequence of:
1. conversion of information into matter
2. material interaction
3. transmission of information
"the way a phenotype responds to selection pressures depends on how it's made."
Key innovations can make prediction difficult, often originate due to gene or genome duplications ->
historical component
HOX -> influence formation of patterns along the anterio-posterior axis -> HOX gene duplications!
Segmentation: allows change the function of some body parts
Tissue architecture and cancer: cancer -> consequence of unwanted evolutionary process (several
somatic mutations in the same cell lineage, these mutations occur most while DNA replication and
cell division. So constantly renewing tissue is more in danger)
Tissue organisation: stem cells and transit cells -> 1 stem => 1 stem and 1 transit; 1 transit => 2 transit
Which developmental process leads to the optimal tissue architecture? Individuals with a suboptimal tissue architecture have a lower fitness -> level on individual
2 models:
1. assumptions: same mutation rate/k=2N cells/no cell death (k-1 cell divisions!)/at m mutations ->
cancer/all mutations dominant
Take cells with least mutations! Nearest to origin
2. assumptions: single stem cell ->! k=2N cells/m=2 or 3 lead to cancer/stem divide n1 times/transit
divide n2 times/n1=2N-n2 -> n1 increases exp. As n2 decreases
Stem cells are less exposed, less mutations!
K = n12n2 total cells
Modulations if: a) all cell divisions same mutation rate -> minimise lineage length!
b) stem cell divisions have lower mutation rate -> make longer stem cell lineage!
c) k changes -> change the ratio!
Stem cells -> less exposed, go into apoptosis when damaged, radio-protected = lower mutation rate
in stem cells!
Self vs. Foreign recognition mechanisms:
To control cells and particles a self vs. Foreign recognition mechanism needs to evolve and develop ->
needs to recognise and respond appropriately -> thanks to diversified genetic systems -> but somatic
mutations can be risky, must be controlled!
If the mechanism is:
1) too sensitive: auto-immune effects/attack of conspecific tissue -> infertile!
2) not sensitive enough: defence not compromised!
Traadee ooooffff
Evolutionary processes -> development
Maternal control and morphological diversity: maternal mRNA: minimal gene expression by the early
embryo/can extend to the moment of germ-line sequestration
Proliferation-induced mutagenesis ->
Genomic conflict and genomic imprinting
Intragenomic conflict:
Same individual, different loci, same time; it is genetic conflict within an organism (transposable
elements = genetic parasites)
Conflict arises because:
1) not all genes are transmitted in the same way (by one sex, eg mitochondria)
2) not all offspring inherit the same set of genes (genes that can influence fair meiosis -> transmission
advantage)
Genetic level/individual level! T-haplotype in mice!
Selfish genetic DNA = genetic parasites: genes that cause intragenomic conflict, can be harmful, leads
to selection of restorer and suppressor genes, always new "troublemaker"
Transposable elements: make up 35% of mammalian genome, that's a lot! Two types: 1)
retroelements 2) DNA elements. They can replicate within the genome ->
1) reverse transcriptase
2) excision and insertion
Chance increased on next offspring. Transposable elements can lower the fitness of host, can also kill
it (into coding or regulatory sequence)
Do not occur in somatic cells, would also harm theirselves. Self-splicing -> jump out in right moment.
Are sensitive to cellular environment, can be useful!
DNA methylation maybe involved in silencing of transposable elements -> decrease in DNA
methylation ddm leads to uncontrolled release of many transposable DNA -> because of insufficient
methylation!
Cytoplasmic genetic elements:
They don’t segregate as precisely as the nuclear genes, eg mitochondria.
But it can be adjusted by subsequent (folgende) multiplication. If a mutation in cytoplasmic element:
the competitively superior form is “favoured”, becomes established. But: if disadvantage to host ->
no establishment.
During sexual reproduction: different cytoplasmic genetic elements fuse. Mitochondria: sperm
doesn’t pass it on, its mitochondria is tagged for destruction. But: there may be competition (if there
are sampling errors which lead to different mixes), and the superior will establish, even if this harms
the individual!
They usually have uniparental inheritance -> mother, anisogamy! Father –> ubiquitin for degradation.
But: also occurs in isogamous species! So, uniparental inheritance reduces conflict of cytoplasmic
genetic elements. But: leads to another genomic conflict: men are a dead end. So the female fitness
may be enhance at the expense of male fitness or the sex ratio may shift towards the female site ->
nuclear genes to counteract the effects of the cytoplasmic gene -> sex chromosomes?
EXAMPLE 1: cytoplasmic male sterility
Gynodioecious = hermaphrodites & females, females = male-sterile hermaphrodites (no viable
pollen)
Male sterility -> mitochondrial mutations! So they produce a higher yield (Ertrag) due to the trade off
(invest more in female function). They are easier to cross, easier to hybridise -> crop plants.
Why was this established? Mitochondrial mutations which lead to decrease in male function -> good
for mitochondrias! They are passed on via female function! “Indeed, a mitochondrial mutation that
eliminates male function while enhancing the female fitness of its carriers will be favoured, for the
fate of mitochondrial genes is affected only by their carriers’ female fitness.”
Plantago coronpus: restorer alleles -> restore the effects of cytoplasmic genetic elements. “the
number of restorer alleles correlates with the proportion of hermaphrodites in the population (the
sex ratio)” -> the more pollen, the more restorer alleles!
EXAMPLE 2: genomic imprinting
(intergenomic?) genomic imprinting is parent-specific gene expression = expression depends on from
father or mother, father and mother disagree which gene active/passive. Most of these genes are
linked to growth. Optimal amount of resource supply! Father and embryo want everything now,
mother not for later pregnancies. Through methylation mother switches off the “shout” gene.
Asymmetric kin -> “for some genes the paternal copy is expressed and the maternal copy is inactive”,
so it is an unfair distribution! Imprinting prevents parthenogenesis! A parthenogenetic mutant
couldn’t express all genes! Genomic imprinting evolves at the level of an allele –> “natural selection
favours different levels of expression depending on an allele’s sex-of-origin in the previous
generation” Woher kommt das exprimierte Allel, Mutter oder Vater?
IGF2/IGF2r -> father: igf2 -> insulin growth factor, fetus “asks” for more nutrients, only paternal copy
is active, maternal inactive/mother: igf2r -> receptor which inhibits igf2, only maternal copy is active,
paternal inactive. “selection for these two genes acts in opposite directions in males and females,
thereby creating a remarkable genomic conflict between paternal and maternal genes whose effects
occur in the offspring.” How would this work in sea horses?
Green Beard
 Signal their presence in an organism (feature)
signalisieren
 Detect the presence in another
(perception) erkennen
 Help the carriers of such genes
(response)
helfen
Mother – embryo -> placenta. When embryo signals that it has got the green beard allele, mother
can provide it, even at expense of the other embryos and thus the mother -> gestational drive
Cadherin -> cell-cell contact, involved in response (gene activation)
But: the evolution of suppressors is expected, leading to antagonistic coevolution!
There is an establishment of cadherins involved in maternal-foetal interaction -> likelihood of fixation
Genome evolution
Genome size: eukaryotes: smallest = 0.0023 pg, 1 pg = 109 base pairs, largest = 1400 pg
Increase in the amount of DNA? 1) de novo synthesis of sequences that are not homologous to any
pre-existing DNA 2) duplication of pre-existing DNA
Three main mechanisms: unequal crossing over/transposition/polyploidisation
Four possible fates of duplicated loci:
1) One copy is inactivated and slowly degrade
2) The two loci diverge, while maintaining similar functions
3) The loci diverge and acquire different functions while still maintaining somewhat similar to
protein 3D structures
4) One copy acquires a new function after a frame-shift mutation (little sequence homology)
Changes in chromosome form -> all known mechanism require at least two chromosome breaks!
Translocation/centric fusion/paracentric inversion/pericentric inversion
Effects of changes in chromosome structure: heterozygotes for the new structures have reduced
fertility -> half of the gametes are aneuploid (a gene is copied twice, another is missing)
Repeated DNA:
 Gene clusters
proteins -> different codes, diversification!
 Tandemly repeated genes
allow high volume production
 Tandemly repeated DNA
useful genetic markers
 Middle repetitive dispersed DNA
dispersed throughout the genome
 Highly repetitive DNA
arranged in tand. rep. blocks
Haemoglobin: embryos/foetus/adults -> different peptides for different oxygen requirements!
-> Exons/introns
Coevolution
Definition:
 Coevolution can occur if part of the environment of a species is shaped by a specific set of
genes of one or several other species
 The intensity (i.e. fitness effects) and frequency (i.e. the spatial and temporal patterns) of the
interaction are important parameters for coevolution
 Only if both parameters are high we expect highly specialised interactions to evolve
 Extended phenotype
 Coevolution ist abhängig von Umwelt sowie der umgebenden Spezies, welche diese verändern.
Zwei wichtige Parameter dabei sind: Intensität (Fitness Effekt) und Frequenz (räumliche und zeitliche
Muster). Nur wenn beide Parameter stark sind -> hoch spezialisierte Interaktionen coevolvieren.
Extended Phenotype = erweiterter Phänotyp -> alle “Effekte eines Gens” auf die Welt, im Phänotyp
werden die Effekte als begrenzt auf den Körper betrachtet
Mutualism ++/parasite-host; predater-prey +-/competition --/commensalism0+/by-product 0Whereas the last two are broad-sense coevolution -> only one of the partner evolves in response
Costs and benefits of interactions are difficult to measure and may depend on environment. The
interactions may vary spatially and temporally. Variation in symmetry. Sampling over several
populations for signs and strengths -> gene flow!
Levels of coevolution:
Genetic elements WITHIN organism/ancient symbioses/males and females/parents and
offspring/coevolving species/coevolving clades/coevolution of GENES and CULTURE
Inter- or intraspecific!
Example: star orchid with floral tube ->moths may evolve longer tongue than needed -> pollen
transfer, predators sitting on plant
Deceptive pollination in orchids: batesian floral mimicry (flowers mimic a particular rewarding
model)/sexual response (flowers mimic female mating signals)/pseudoantagonims (plants invoke
defence mechanism, mimic enemy)
Bitterlings and Unionid -> bitterling lays eggs in mussel, mussel larvae grow on fishes -> mutualistic,
but: bitterlings are poor hosts due to prevalence, infection intensities, retention
Kidneyshell -> larvae look like small fishes
But: no clear evidence for coevolution response because: not ver high specificity; very costly,
asymmetrical interaction
Two examples for mimicry (in Vorlesungsskript mehr)
Aggressive mimicry
Predator disguises himself as something harmless or even desirable. Example: blister beetle ->
juvenile disguise as female bees in shape and size, release an odour -> transfer to the male -> male
copulates with female -> transfer to female -> transfer into nest
Batesian mimicry
An edible species (the mimic) evolves to resemble a warningly coloured noxious species (the model)
Selection on batesian mimicry is mediated by predators that avoid mimics. The convergence of the
mimic to the model is limited by the sensory system of the predator. The cost of eating a model
must be higher than the benefit of eating a mimic. May lead to learning in the predator. Fitness
advantages of mimic are frequency-dependent (space and time). Happened a lot independently
Four criteria for coevolution:
The selection/perturbation/functional/design criterion
Coevolutionary origin -> resulted from reciprocal evolutionary change!
Sexual Selection
Anisogamy/isogamy, later is probably the ancestral condition
Evolution of anisogamy -> disruptive evolution one gamete specialises in swimming, other in
providing energy, selection against fusion between two small cells (not viable!) and against fusion
between big cells -> too expensive! Small cells compete for access to large cell  sexual selection
Sexual selection: Darwin: not struggle for existence in relation to other organism, struggle between
the individuals of ONE SEX. Result not death -> few offspring
Jennions and kokko: sexual selection favours investment in traits for more offspring, competition of
members of the same sex.
Sexual selection  survivorship + fecundity + mating success = fitness
Bateman:
females 
reproduction limited by the number and quality of eggs produced
Males 
reproduction limited by the number and quality of eggs fertilised
Females: dependent from resources, males: dependent on number of females
Two basic types of sexual selection: male – male competition = intrasexual selection/female choice =
intersexual selection
Female choice does not need to be a conscious decision nor increase female fitness
Mating systems: monogamy/polygyny (harem)/polyandry (one female, lots of males)/polygamy (both
sexes several partners)
Social mating system ≠ genetic mating system  bastard, in humans every 20th not father child
means it is
Measurement survivorship etc  variance for quantitative measurement: eg red deer, mean of
female/male = 7.5, variance female = 6.1, variance male = 38.7!!
Fisherian runaway process: costs of female choice stop the run
Handicaps, indicators and good genes: females prefer males with traits that indicate good genetic
quality, but quality is expected to be already under directional selection  what maintains the
variation in male quality?
Direct effects: females prefer males that provide material benefits  can be measured
Sensory exploitation: males exploit an existing sensory bias in females eg preference for red dots
because female like red berries
Can be starting of fisherian runaway process, females can’t easily evolve resistance against this kind
of exploitation!
Intrasexual  contest competition, fight, winner gets the girls.
Intersexual  MHC genotype, men without are more attractive
Pre- and postcopulatory level: scorpion flies  bigger gifts = longer copulation = larger sperm
transfer
Sperm competition: competition WITHIN a single female, between the sperm of two or more males
for the fertilisation of the ova  not fighting sperm, rather competition between ejaculates
Risk/intensity model:
The link between sperm mixing patterns and paternity can lead to: evolution of: sperm
number/sperm size and speed/manipulating genitalia
Testis size/body weight are linked linear
Cryptic female choice: female-controlled process or structure that selectively favours paternity by
conspecific males with a particular trait. The dismissed  lack of trait
Non-random paternity  resulting from female morphology, physiology or behaviour that occur
after copulating
Does not have to be a conscious choice!
So: sperm competition + cryptic female choice = sexual conflict
Sex allocation
Fisherian sex ratios:
blue = male investment in offspring
In relation to 50:50 distribution  unfair! Amount of resources should be equal
Two-fold cost of sexual vs. parthenogenetic reproduction is a direct consequence of fisherian sex
ratios
Darwin: when one population too many males (of the useless)  natural selection: females which
produce more females favoured  equalisation  level of individuals
But: revision: problem: so intricate that it is safer to leave its solution to the future  level of species
Which processes select for deviatons of the 1:1 fisher sex ratio? Individual level?
Sex allocation theory:
 predicts the optimal investment to male and female reproduction
o sex ratio in gonochorists, sex order and timing of sex change in sequential
hermaphrodites, allocation to male and female function in simultaneous
hermaphrodites)
 predicts the optimal sexual system
o gonochorism or dioecy? Sequential or simultaneous hermaphrodites? Mixture
(androdioecy)?
 Predicts the existence of plasticity
o Plastic sex allocation in response to the environment may be advantageous under
some conditions  environmental sex determination
Gonochorists  fig wasps  are haplodiploid, so incest no risk  when equal sex ratio  local mate
competition! So it’s advantageous to make a maternal sex-ratio adjustment. When other mothers 
more sons as coverage  the more foundresses, the more the ratio approaches 50:50
Local mate competition in the parasitoid wasp nasonia  sex-ratio in relation to first female, second
lays a lot more males!
Trivers and Willard hypothesis: males in polygyny have a higher variance, male reproductive success
depends on male condition, high condition monopolising, low-condition males unmated
Female reproductive success also depends on condition but less strongly than for males, mother in
good condition will produce offspring of good condition  should preferentially produce more males
Social rank  the higher the better the reproductive success, the more male offspring
Sex change: protandrous (male to female)/protogynous (female to male)/bi-directional
Small males more successful than small females, but big females better than big males
Small males less successful than small females, but big females less than big males
Protandry  clown fishes, female fecundity is strongly size-dependent, so largest individual should
be female! Or slipper limpet  one on top is male, between are intermediate forms
Protogyny  reef fishes thalassoma bifaciatum with terminal phase fishes and initial phase fishes
(resemble females). Small reefs: at best site are the TP males, small males are not competitive, IPs
occupy group spawning site, streaking or sneaking. Big reefs: more fishes in site, TPs can’t cover all,
IPs in group-spawning. Reproductive success of IPs are here equal to the success of females, TPs still
very high.
The bigger population size, the less TPs. Smallest reef, smallest population has NO IPs.
IPs have bigger testicles  high investment in sperms!
Parasite-induced sex change in thalassoma bifasciatum 
females infected with myxozoan, sporulate in eggs, destroy a
proportion of offspring  female is forced to change earlier, at a
smaller size and lower fecundity
Bidirectional sex change  polychaetes (ophyrotrocha) form pairs, smaller one is male. But males
have higher growth rate  when bigger, sex changed  pair might end up as simultaneous
hermaphrodites
Sex allocation in simultaneous hermaphrodites  fitness gain curves, saturating male fitness due to
sperm competition. So invest in male function until saturation, then invest “rest” of resources in
female function  female-biased sex allocation  selfing rate  monogamy has same effect as
selfing
But: higher sperm competition linearises the male fitness gain function  male allocation increases,
female decreases  more males
Local mate competition model:
assumes trade off  the more competition, the more
male allocation, the more individuals, the more 50:50
Small group  big ovary
Big group  small ovary
Effect of brooding: brood pouch may limit the female function, remaining resources to male function
 male-biased sex allocation possible
Disadvantages of sex change: cost (lost time), impossible when physiology or morphology complex,
learning and training
Disadvantages of simultaneous hermaphrodites: costs, high sexual specialisation required for
gonochorism, phylogenetic patterns
Sexual conflict
Intergenomic/intersexual ontogenetic
Intralocus sexual conflict: occurs when negative correlation between the selection coefficients of the
same allele when expressed in male AND female; sex specific selection, but disadvantageous in other
sex  hip width
Interlocus sexual conflict: occurs when adaptive replacement for male’s success also reduces lifetime
fecundity in females; counter-adaption at a locus, influences female fitness because it protects her
from male-induced harm. But bad for male’s success.  sexually antagonistic coevolution between
same loci
Intrinsic conflict over mating rate: sexes different levels of parental investment in offspring. Distinct
from interlocus unless adaptions reduce female’s lifetime fecundity
Intralocus:
Can be reduced by sex-limited gene expression  Pfau, secondary sexual characters
Fitness of drosophila melanogaster of different haplotypes differs depending on the life-history stage
 the fitter male in juvenile, the fitter juvenile female; the fitter adult male, the less fit adult female
Interlocus:
Conflict over optimal mating rate/conflict over investment in current vs. future reproduction (broodcare)/conflict over usage of sperm and paternity
Male manipulation: increase of refractive period/stimulate egg production (most successful)/lethal
manipulation
Male persistence and female resistance can coevolve!
Genital morphology  bring females early death, force them to use all resources in current event.
But: genital morphology more for sperm removal
Infanticide and cannibalism  can be advantageous to be eaten!
Seminal fluid proteins  induce oogenesis and ovulation; influence female remating rate; are
required for correct sperm storage; influence hatching rate  influence behaviour and physiology!
AND they are toxic for females!
Female reproductive tract  same in all fly groups, but fluid proteins not!
Sex peptide fluid  induces ovulation; causes one week suppression of remating, but only if only
sperm are transferred  bound to sperm!  long sperm, due to release from tail region via
enzymatic cleavage
Sperm - egg interactions: sperm should be less choosy  rapid fertilisation due to sperm competition
 fast evolution of genes involved in gamete recognition and fusion
Sexual conflict and speciation: due to sexual conflicts  repr. Behaviours, morphology and
physiology evolve very fast  reproductive isolation can evolve quickly too  sexual conflict speeds
speciation process up!
Summary: intralocus = hip width, genetic correlation between haplotypes; interlocus = genital
morphology, infanticide and cannibalism, seminal fluid proteins, sperm-egg interactions, sexual
conflict and speciation
"rivers and Willard (1973) first proposed a verbal model for polygynous mammals in which a mother
may allocate offspring to different sexes according to her condition: male-biased investment when
she is in good condition and female-biased investment when she is in bad condition. In polygynous
mammals, high-quality mothers should get much larger fitness returns (number of grand-offspring)
from high-quality sons than high-quality daughters by their extra investment because of strong
male–male competition for mating"
Sex in Simultaneous Hermaphrodites
Distribution: in about 70% animal phyl; only 5-6% of the animal species
Advantages: reproductive assurance/low density (potential mating partner)/local mate competition
(limited male-male competition)/local sperm competition  favour a female-biased sex allocation
Sim. Herm. Often have a higher female than male investment!  female biased!
Brooding  remaining resources when brood space full  for male function
Local resource competition when offspring compete among themselves for common resources,
invest the remaining resources in the male function
Last two favour male-biased sex allocation!
Darwin doubted that sexual selection occurs in sim hephr.  but he was only aware of precopulatory sexual selection  post-copulatory: sperm competition and cryptic female choice
Bateman's principle in gonochorists: males want to mate more often than females (in males
reproduction is limited by the number of eggs fertilised)
Now in sim. Herm.: Charnov: they want to give more sperm than rather receive it  many
hermaphrodites are expected to have a preference for the male sex role
Cross terms  mating good for male sites but bad for female sites, mating often in female, but
decrease in male function, not really sexual conflict
In gonochorist: mated female may not want to engage in additional copulations  avoiding males
avoids sexual conflicts
In sim herm.: femal function of a mated may not want to engage in additional copulations  female
function wants to avoid additional matings, but the male function of the same individual will want to
continue!
Sexual conflict: incompatible mating interest  scheme! Mating should take place if net benefit is
positive. Possible solution is reciprocal mating  giving sperm is conditional with receiving  lead to
sexually antagonistic coevolution (arms race) between 1) adaptations in the recipient that allow to
remove sperm in such matings  cryptic female choice 2) counter adaptations in the donor that
prevent sperm removal  male persistance
Egg trading in hamlets: take turns! Risk of cheating
Conditional sperm receipt: reciprocal behaviour  lead to fertilisation trading?
Cryptic female choice: digest  forced to cheat
Hypodermal sperm donation  stabs holes