UNIT 3 ALL lec

Wolbachia 1

a common bacterium that lives inside the cells of arthropods. They infect 2/3 of the world’s arthropods. Passed onto offspring via infection of the egg (but not sperm).They have a range of reproduction-manipulating mechanisms

What is cytoplasmic incompatibility

a reproduction-manipulating mechanism that helps ensure that the Wolbachia strain continues to reproduce and spread.

Infected males can only reproduce with what?

Infected females with the same strain of Wolbachia

What would infected males (w/wol) mating with a unaffected female do?

Their embryo would die early and this also happens in different strains mating

What can wolbachia be used effectively to do in mosquitoes?

Effectively eradicates the mosquitos which controls the spread of infectious diseases disproportionately affecting rural ethnic populations in Asia and Africa.

What are examples of disease that the eradication of mosquitos can effect via transmission rates?

Dengue, Zika, Malaria

Wolbachia does what in mosquitos? And what are the long-term practical applications?

Induces Sterility, this can lead to male mosquitoes leading to early embryonic failure in females and as a result reduces the population by 94%

Wolbachia can do what to male embryos and why is this an issue? (all insects)

They can feminize embryos which leads to a disequilibrium in sex-ratio which is not ideal.

Wolbachia can do what to females(in all insects)?

It reduces female fecundity

How does Wolbachia transmit?

through both somatic and germ cells, replicating as the host’s cell replicates

Genome is considered as a

integrated and cooperating set of genes that has evolved under selection to maximize fitness.

what kind mutations are common?

Mostly reducing survival and reproduction ,and the mutations are eliminated by selection, and the less common beneficial mutations are favored by selection

What are selfish genetic elements?

They are stretches of genome that gain increased transmission relative to other portions of the genome, but they are either selective neutral or detrimental to overall organismal fitness with rarel an external effect on phenotype.

Why do selfish genetic elements happen?

genes in a single organism do not always agree with he best outcome obvious by the fact they can spread in a population despite harmful effects overall to the organism , this is also known as intragenomic conflict.

What did the existence of SGE affect our understanding of genomic transmissiom?

It centers the genes-eye view over considering the entire genome together

Intragenomic conflict

Genes or stretches of genome function to increase their own transmission to the detriment of other genes or stretches of genome in the same genome

Selfish genetic elements of SGE

these include stretches of DNA that gain increased transmission relative to the rest of the genome: Often detrimental to the organism’s fitness, Have evolved many times across the tree of life, Have diverse mechanisms for gaining a transmission advantage

Genetic Drive

when a genetic element is transmitted at higher rates to progeny
than by mendelian expectations. (i.e. not a 50:50 chance).

What are the general mechanisms for achieving drive include?

Interference, Overeplication, Gonotaxis,

Interference

Disrupts transmission of alternative allele

Over replication

replicated more than other genes via transposable elements and sometimes mitochondria or chloroplasts can do so

Gonotaxis

move preferentially towards the germline away from somatic
cells (segregation distorters)via Female meiosis gives rise to one functional egg and 2-3 polar bodies. Competition to be included in the egg has led to knobs on chromosomes of maize, which act as centromere during meiosis and pull themselves along the spindle.
and When segregation distorters occur on sex chromosomes, they can
skew the sex ratio (but often opposed by another selective force)

What is rule 1 of selfish genetic elements?

Highly self fertilizing or asexual genomes should experience less conflict between selfish genetic elements and the rest of the genome. This requires sex and outbreeding

Consequences of rule 1 of SGE

Sexual reproduction places selfish genetic elements in new genomes, rather than being stuck. Being stuck means that lineages with fewer selfish genetic elements will often outcompete those with them.Increased homozygosity in selfers reduces competition among homologous
gene regions greater linkage disequilibrium in selfers will sometimes select for reduced transposition rates

Rule 2 of SGE

often hard to detect selfish genetic elements in natural populations, but in hybrids, you can detect the phenotypic consequences as a result, it’s revealed in hybrids

Outcome of SGE rule 2

selfish genetic elements often go to fixation rather quickly, but having
offspring with and without SGE allows us to detect their presence, hosts have evolved mechanisms to suppress SGEs (e.g. small RNA
administered silencing of transposable elements). Co-evolution between
suppressors and SGEs can be very rapid (think Red Queen Hypothesis).
Hybrid offspring can inherit the SGE but not the suppressor

what is the main types of selfish genetic elements?

Transposable elements, Biased gene converters, B chromosomes, Selfish mitochondria, and Meiotic drivers

What are transposable elements?

Genetic sequences that can move to new positions within a genome. They are among the most successful types of selfish genetic elements and often contain all the coding necessary for their own movement.

Who discovered transposable elements and when were they recognized for this work?

Barbara McClintock discovered them in maize. She was awarded the Nobel Prize in Physiology and Medicine in 1983 for this discovery.

How do transposable elements typically move within the genome?

They excise a portion of the genome and then "repair" it with a copy of themselves (cut and paste mechanism).

What are the potential effects of transposable element insertions?

Most random insertions are relatively harmless, but they can disrupt critical gene functions. Transposable elements have been linked to various human diseases, from cancer to hemophilia.

How common are transposable elements in different organisms?

They comprise between 30-80% of the genome in many animals and plants. Specifically: 50% of the maize genome, 45% of the human genome, 15% of the Drosophila melanogaster genome, 0-21% in bacteria, depending on exposure to other lineages

What can happen to transposable elements over evolutionary time?

They can get "frozen" in place and become inactive, after which it takes millions of years for them to evolve away from the genome.

What is the typical fitness impact of transposable elements?

They generally have low negative impacts on fitness. In some cases, they can even be beneficial, such as contributing to adaptive changes in Drosophila and dogs.

How can transposable elements benefit bacteria?

In bacteria, transposable elements can be beneficial when plasmids carry genes for antibiotic resistance.

What are biased gene converters (converting elements)?

Genetic elements that preferentially insert into homologous (uninserted) sites in the genome. They are also known as homing endonucleases.

How do biased gene converters work?

They cleave at specific 15-20 bp sequences and then repair the cleaved area with their own gene using endonucleases.

What is the likely origin of biased gene converters?

They likely originated from a functional process (DNA repair).

Where in the genome are biased gene converters typically found?

They are found in areas of the genome that have high recombination rates.

What caution should researchers take when studying biased gene converters?

They can mimic the effects of selection on genome studies, potentially leading to misinterpretation of evolutionary patterns.

How is modern technology related to biased gene converters?

CRISPR-Cas9 technology allows for the artificial construction of these systems (homing endonucleases).

What are meiotic drivers?

Genetic elements that bias their own transmission through meiosis, resulting in inheritance at higher rates than expected by Mendelian inheritance (50%).

What is true meiotic drive?

True meiotic drive occurs when there is preferential segregation to the functional egg pole during gametogenesis.

What are gamete killers?

Genetic elements that cause selective elimination or functional disruption of gametes that don't contain the driving elements in their genome.

In which sex are gamete killers typically found and why?

Gamete killers are typically found in males because they can afford to waste gametes more than females can, as females produce fewer gametes overall.

How do gamete killers affect fertilization rates?

They result in increased fertilization of eggs by sperm with the driving chromosome from heterozygous males.

How does a killer gene (K) increase its transmission?

The killer gene 'K' is able to kill non-K bearing sperm, thus increasing its chances of fertilizing an egg.

What are B chromosomes and what are their basic properties?

B chromosomes are additional sets of genes that are not required for viability or fertility. They can persist in populations and accumulate due to their ability to self-propagate independently of the rest of the genome.

How do B chromosomes vary within species and how common are they across different organisms?

B chromosomes often vary in copy number between individuals of the same species. They occur in approximately 15% of eukaryotes, being common in eudicot plants, rare in animals, and absent in birds.

What is the basic conflict involving selfish mitochondria?

Selfish mitochondria represent a genetic conflict between typically maternally inherited mitochondria and biparentally inherited nuclear genes.

How do selfish mitochondria manifest in hermaphroditic plants?

In hermaphroditic plants, mutations in mitochondria that affect resource allocation toward female reproductive functions improve the chance of mitochondrial transmission, as producing pollen is an evolutionary dead end for mitochondria.

What is cytoplasmic male sterility and its evolutionary implications?

Cytoplasmic male sterility is the loss of male fertility. In species where this occurs, nuclear genomes have evolved restorer genes that repress the effects of cytoplasmic male sterility genes, creating an evolutionary arms race.

How can selfish mitochondrial effects be detected in hybridization experiments?

Selfish mitochondrial effects can be detected by crossing individuals from different species that have different combinations of male sterility genes and nuclear restorers, resulting in hybrids with a mismatch between these genetic elements.

What are three population-level consequences of selfish genetic elements?

1) Species extinction through biased sex ratios 2) Speciation through reproductive isolation 3) Genome size variation (contributes to C-value variation among species

How can selfish genetic elements contribute to speciation?

By causing changes in morphology/life history and through coevolution between SGEs and suppressors leading to reproductive isolation. Example: P element in Drosophila causes reduced fitness in offspring when P-carrying males mate with females lacking P elements.

How do SGEs contribute to genome size variation?

Two types of SGEs - B chromosomes and transposable elements - contribute significantly to genome size variation (C-value). This variation is poorly correlated with gene number or organismal complexity (animals vary 7000-fold, land plants 24000-fold).

What are three practical applications of selfish genetic elements?

1) Plant breeding using cytoplasmic male sterility 2) Genetic manipulations using transposable elements 3) CRISPR gene drive for targeted genetic modification

What are the two main mechanisms of meiotic drive?

1) Gamete killing in males - drivers within inverted sequences kill sperm lacking the driver 2) Gonotaxis in females - preferential transmission into the ovule

What is the t haplotype in mice and how does it function?

The t haplotype is an autosomal meiotic driver that kills/disables sperm not containing it. It spans more than 1/3 of chromosome 17, comprises >1% of the mouse genome, and has existed for 3 million years. Homozygotes (t/t) die in utero.

How is CRISPR technology being combined with selfish genetic elements?

CRISPR allows construction of artificial homing endonucleases. Now being combined with transposons to more efficiently target sequences (though currently only demonstrated in bacteria).

What are the two fundamental rules of selfish genetic elements?

1) SGE diversity correlates with outbreeding rate (sexual reproduction increases spread, inbreeding decreases spread) 2) SGE phenotypes are typically revealed in hybrids but not within-population crosses

How do selfish genetic elements influence eukaryotic evolution?

SGEs: 1) Contribute to host speciation via hybrid sterility 2) Can cause host extinction through sex ratio distortion 3) Shape genetic architecture (large portion of genome) 4) Drive gene duplications via transposons 5) May drive evolution of mate choice

How might selfish genetic elements influence mating behavior?

SGEs can drive mate choice for genetic compatibility (e.g., t haplotype in mice) and promote polyandry, as females mating with multiple males can avoid passing on selfish elements (carriers have compromised sperm competitiveness).

intrinsic conflict over mating rate (does not count as sexual conflict)

occurs when the sexes have different levels of parental investment in offspring; this intrinsic conflict is an integral part of the process of sexual selection (because of anisogamy), but it is distinct from interlocus sexual conflict, unless adaptations by males to fertilize a female’s eggs also harm the female by reducing her lifetime fecundity

interlocus sexual conflict

ccurs when: (i) an allele coding for a trait that increases male’s success in sexual selection simultaneously reduces the lifetime fecundity of females that interact with him, and (ii) there is counter-adaptation at a locus that influences a female’s lifetime fecundity, because it protects her from male-induced harm but consequently reduces the success of any male with whom she interacts in a reproductive context, this coupling of selection at the interacting loci perpetuates sexually antagonistic coevolution
between these same loci

What often occurs interlocus sexual conflict in male adaption?

(sometimes but not always involved in male-male competition)
that interrupts/limits female mate choice

Examples of interlocus sexual conflict

Cannibalism and Infanticide

Infanticide

Female lions are sexually unreceptive when caring for cubs so a new lion in the pride kills them to make them more perceptive to mating, also happens in some spiders where they steal 33% of the egg sac and eat it

Sexual Cannibalism

looks like sexual conflict when the cannibalized sex has a lower mean fitness bc they lose future reproductive opportunities because of loss of future mating, when it isn’t sexual conflicts is when the same thing happens but there is no loss in future copulations (Dolomites fishing spiders)

Genital morphology

Males could try to bring females into a terminal situation by
harming them so that they will not live much longer. Females could thereby be forced to invest all their resources in the current reproductive event.

Seminal fluid protiens

Male manipulation of females which up regulates female egg laying rates and reduces her desire to re-mate with another male(serving the males interest), but shortens the females lifespan

Sperm Egg interactions in external

sperm should be much less choosy with whom to fuse than the egg.
because a hybrid between two closely related species may have greater than zero fitness and because sperm competition selects for rapid fertilization, this is expected to lead to fast evolution of genes involved in gamete recognition, similar processes may also act in internal fertilizers

Sexual conflict occurs at which stages

before, during copulation, during insemination, after pair bonding.

intralocus sexual conflict

natural and sexual selection favor different fitness optima in each
sex, the sexes share a common genome, and sex-specific gene expression is not perfect, so genes favored by selection on males/females are often expressed in the opposite sex, where they are detrimental. Genomic tug-of-war. Can be resolved when sex-limited gene expression evolve. Or, there could be a middle ground (e.g. hip width of males and females in humans

What are the circumstances of intralocus sexual conflict

when there is a negative correlation between the selection coefficients of the same allele when expressed in males and females, leads to negative genetic correlation between male and female fitness, sex-specific selection at a locus in one sex interferes with adaptation at the same locus in the other sex, Can be solved by sex-specific expression of phenotype

At what time does intralocus conflict occur in flies and lizards?

only in adults for flies as sex-specific gene expression may be stage-specific, in lizards testosterone starts maturity and resolves intralocus conflict over body size as adults by altering the expression of size-related genes in males and female.

Cryptic female choice allows females to

allocate sperm from large males to fertilize male offspring, but allocate sperm from small males to fertilize female offspring

Males with genes that increase body size are better at

male-male competition, but their daughters are at a disadvantage because small females have higher fitness.

What is unique to human placentas?

They have the most invasive genetalia

What is the parent-fetus genetic conflict and its general outcome?

The genetic conflict between maternal and paternal genes dictates many aspects of pregnancy. While this balance typically leads to normal growth and development, it can play a role in pregnancy complications. The offspring contains a mix of maternal and paternal genetics with different evolutionary interests.

How do maternal and paternal genetic interests differ during fetal development?

Maternal genes balance fetal growth with the mother's survival and resources for future pregnancies (glucose, protein, iron, calcium, energy for child-rearing). Paternal genes don't need this balance since gestation occurs in the female and there's no guarantee future maternal offspring will carry paternal genes, so they encourage maximizing resources for the current fetus.

How do maternal and paternal genes influence fetal growth differently?

Paternal genes encourage aggressive fetal growth, quick development, and securing more maternal resources. Maternal genes limit growth to only what's necessary for proper development while preserving maternal health and resources.

What is the placenta's role in parent-fetus conflict?

The placenta is responsible for all resource transfer during pregnancy and is dominated by paternally expressed genes. It releases paternally derived insulin-like growth factors that reduce maternal insulin sensitivity and hormones that increase maternal blood pressure—both increasing fetal resource access but potentially harming maternal health.

What pregnancy complications can result from parent-fetus conflict?

The conflict can contribute to pre-eclampsia, gestational diabetes, miscarriage, and preterm birth.

How does parent-fetus conflict affect birth timing?

Maternal genes favor earlier birth before the fetus grows too large for safe delivery (human maternal pelvis barely allows passage compared to chimps). Fetal genes favor extending pregnancy to gain more weight. The outcome is a compromise balancing costs/benefits for both parties.

How does parent-fetus conflict contribute to gestational diabetes?

The placenta provides nutrients to the offspring and produces hormones (estrogen, progesterone, cortisol, human placental lactogen) that affect insulin use. As the placenta grows, it produces more of these hormones, increasing insulin resistance. If the pancreas cannot produce enough insulin to offset this increase, gestational diabetes develops.

What are the mechanisms behind early and late onset preeclampsia in relation to parent-fetus conflict?

Placental tissue (influenced by fetal genes) invades maternal uterine arteries, affecting arterial plasticity and blood supply. Early onset preeclampsia (<34 weeks) occurs when invasion is inadequate, causing placental stress and reduced blood flow. Late onset preeclampsia (>34 weeks) relates to maternal cardiovascular defects and inflammatory responses to placental metabolic byproducts.

Adaptions

are the process by which a species becomes fitted to its environment; it is the result of natural selection’s acting upon heritable variation over several generations

Coevolution

is the process of reciprocal evolutionary changes in interacting species

Evolutionary stable strategy:

behavioral strategy (phenotype) if adopted by all individuals in a population that cannot be replaced or invaded by a different strategy through natural selection.

ESS must satisfy condition 1

an individual employing strategy A must do better against
another individual employing strategy A than any other strategy;

ESS must satisfy condition 2

should a new strategy evolve (A') that does equally well against
strategy A, for A to be an ESS, an individual employing strategy A
must do better against an individual employing strategy A' than
an individual employing strategy A'

Dove v Dove

resource split

hawk v dove

hawk takes resources

hawk v hawk

resource split, conflict cost

Hawk strategy is an ESS only if the value of the resource is
______ than the cost of the conflict_____.

greater, (B > C > 0)

Extinction rates are _________ than the background extinction rates in fossil records.

significantly higher

Population drive affects by climate change

Annual Population growth rate, population size, local extinction risk

Demographic drive affected by climate change

Annual survival rates, reproductive success, somatic growth rate