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samenvatting tentamen 3 evo devo
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summary of everything that comes back at exam part 3 of evo devo in P4
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Summary Evolutionary Developmental Biology (AB_1141) partial exam 1+2+3
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Lecture and slides notes Evolutionary Development Biology (AB_1141)
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samenvatting tentamen 2 EVO DEVO
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EVO-DEVO tentamen 3 belangrijke punten:22. Ageing
Variation between and within species. It is a decrease ability to survive and reproduce.
Health problems increase with age.
Asymmetry: E. coli with older copy of chromosome > the lower the growth rate. No need of
evolve perfect mechanisms like immortal germline & disposable soma.
Life history perspective: different aspects of the life cycle. Not one life cycle that works the
best. Differences in development time, reproduction, offspring, lifespan
Resource acquisition & allocation: Y-model. Lifespan vs reproduction = correlated response >
trade-off (one improves than ones get worse). Correlated traits in drosophila: body size etc.
or postponed reproduction: late reproduce > longer lifespan (after few generations)
Internal (cancer, metabolic) & external mortality (infection, dehydration). High extrinsic
mortality animals have early maturation! Human evolution (less extrinsic mortality): parental
care, transition to agriculture & industrial revolution
Unusual human life history: long lifespan. Theory of aging:
- Selection shadow: selection on reproduction and reduce with age, early = higher fitness
- Mutation accumulation: weak selection at increased age caused less input to remove
mutations from the population. We have protected environment, a lot people in shadow
- Antagonistic pleiotropy: genes have effect on more traits, one positive and one negative.
Result of evolutionary tinkering: endocrine system. Trade-off lifespan vs reproduction > virgin
flies’ life longer than mated flies. BRAC1: enhanced fertility but enhance mortality. Also
looked into trade of via insulin growth factor (IIS) and results in fertility.
-- disposable soma theory: DNA associated with lifespans (ROS), direct relation
-- theory of aging: gene expression for development and early lifespan. Optimize these genes
at later age increase lifespan without the cost of reproduction. Not always linked.
Aging involves a lot of processes, and inheritably only 15-20%
Treatment ageing: TOR signaling in mice > expanded lifespan but mixed effects on phenotype
Lifespan vs healthspan: aging genes associated with different diseases
23. Gut pathology
Sex and gender differences: differences in morphology, metabolism, health & diseases. This
has important of treatment. Results differences are derived from reproduction
Gut and reproduction: Critical role in nutrients uptake. Female reproduction is energetically
very costly, require adaption. The gut is remodeled, mediated by endocrine signaling
Dietary restriction (DR): no malnutrition but promotes healthy ageing and longevity and
comes with the reduction in reproduction.
Gut epithelial barrier function decline in female lifespan (drosophila), and have ISC (stem
cells) that are sensitive to nutrients.
Age-related gut: the older the more degeneration of the gut. ISC division malregulated with
age in female, leading to proliferation, which disrupts epithelial layers.
Sex differences gut: sex-specific differences in pathology with age, in females this effect
becomes more severe & correlation with high ISC activity.
Sensitivity to infection: males are more sensitive to bacterial infection and pesticides. ISC
activity is increased by infection, and pattern expression between sex and age. Might lead to
a trade of between gut repair and pathology at old age?
Feminizing male guts: create male flies with a midgut of a female, by switching on female sex
determination. looked more like female gut, and more mitosis over age (ISC cells more
active). So leads to more pathologies at higher age. And a stronger response to DR that we
don’t see in normal males. But we do not see a better resistance to bacterial infection in
males with the feminized gut. Because ISC activity is not the only differences in infection
between males and females.
, 24. Brain
The brain increased in jumps. Brain volume increased in homo erectus. Every new species
evolved per specie, not within species. Increase of brain volume is correlated with decrease
of prognathism. Also the skull became more upwards instead of backwards.
Brain volume does not increase linear with body weight. It is related to 0.67 of the body
surfaces. Encephalization quotient (EQ) = brain volume / 0.12W^0.67.
Large increase in neocortex. PFC is the last part that develops in ontogeny and evolution.
Medial PFC: control basic drives. Lateral PFC: temporal organization of behavior.
Limbic system = thalamus, hypothalamus, amygdala, hippocampus > basic function that
comes naturally. Works very close together with prefrontal cortex (PFC). Typically human.
Connection between plesiomorphic (primitive) and apomorphic brain nuclei.
Genetic changes that have influenced the brain evolution:
- Nucleotide substitutions: FOXP2. Involved in language control, got 2 non-synonymous
substations. FOXP2 derived share from neanderthal. No evidence for selection on locus.
- Differential regulation: Human gene expression differs chimpanzee in the cortex and not in
the liver. So upregulation of many genes in the brain. Mostly in transcription factors, involved
in expression of a lot of other genes. So same genes, regulated differently.
- Gene duplication: 1q21.1 genetically instable due to pericentric inversion. Markers for
brain disorders. Examples: DUF1220: unknown function, a lot of copies present in humans.
Correlated to intelligence. SRGAP2: duplicated 3 times, 2 pseudogenes. Incomplete
duplication causes to inhibit the other. Delayed maturation of dendritic spines, more
synapses, molecular neoteny.
- Pseudogene resurrection: NOTCH2NL. Gene conversion now have 3 functional copies.
Stimulating effect on radial glia cells (neural stem cells).
- Human accelerated regions (HARs): regions that are unique in humans. Non-coding, but
bind transcription factor, has effect on expression on other genes. Mostly in
neurodevelopment and cognition. So very different expression than in chimpanzee.
25. Language and cognition
Sensation: Direct experience, qualia also called. Localized in the body.
Sensation + stimulation = perception: sensation is not sufficient. Brain makes perception with
memory. Make image of the environment. Natural selection on this in evolution.
Perception without sensation: uncoupled representation. Like memories or daydreams.
Inner world: stimulate the effect of your actions. No need for trail and error. A total of
uncoupled representations. Great advantage in evolution.
Inner world of somebody else: Theory of mind. Primates are less able to do this.
Self-recognition is required: some animals can, tested via mirror test and some paint. Need
for recognize yourself and realize that they have, to make a cave paint. Only in h. Sapiens
Phycological theory of language: many animals can communicate. Language is a derived
feature. Language is much more, also thinking and image making. Language evolved late.
1. Tools: language is needed for the technique. Able to explain how to make that.
Originated 2.5 Ma BP
2. Position larynx: descends downwards. In human lower so that allows room for space
to make sounds. Australopithecus did not have language, only h. Sapiens.
3. Hyoid bone: less wide shaped in human and bigger frontal part. So cannot speak.
4. Nervus hypoglossals: cranial nerve, that innervates the tongue. The channel is wider
in human and neanderthal than chimpanzee. So, nerve can be thicker.
5. Spinal channel: channel wider for spinal nerve. Goes up to the thorax, that relates to
the lung innervations.
6. Broca’s area: part of temporal. Integrates of capacity of speaking. Connected to
Wernicke’s area. Taung child = fossil with brain, but no Broca’s area.
26 + 27 Defense and pathologies
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