UNIT 3 DAY 6 - WHAT HELPS YOU ALSO HURTS YOU Flashcards
Pleiotropy
single gene that affects 2 or more seemingly unrelated phenotypic traits
antagonistic pleiotropy
gene with multiple effects, 1 beneficial but another harmful
pleiotropy example
sickle cell anemia
Greenwood 2023
deadly diseases left a mark on our DNA –> natural selection in action –> mortality, acting on heritable variation, results in a change in allele frequencies in a population over time
Greenwood 2023 - raising risk of autoimmune diseases
- protective variants that have increased frequency –> antagonistic pleiotropy –> accumulated in a population due to natural selection
genomics
study of all of a persons genes (their genome), including interactions of those genes with each other and with persons environment
DNA
chemical compound that contains instructions needed to develop and direct the activities of nearly all living organisms, made up into a double helix
genome
organisms complete set of DNA
DNA sequencing
determining the exact order of bases in a DNA strand, due to base pairs, researchers only need to know 1 of the pair
Human Genome project
- produced a very high-quality version of the human genome sequence, generates a resource that could be used in biomed studies
- understand genome functions and discovers genetic basis for health and disease
What genomes were examined?
- genomes of 2,879 Europeans (lived between Neolithic period)
- genetic variants that have become common in that time are linked to immunity
- living more densely, increased exposure to infectious diseases (farming and raising animals) –> more exposure to bacteria from farming / animals, diseases can spread quicker
- environmental factors important in spread of diseases
senescene
the process of bodily deterioration that occurs at older ages
how is senescene affected?
- not a single process of bodily deterioration that occurs at older ages
- senescene isn’t a disease but result of every bodily capacity steadily decreases so that we grow steadily more vulnerable to a myriad of diseases
senescene information
- no selection against. genes whos harmful effects only after the oldest age of reproduction
–> force of selection decreases later in life - a gene might be well selected for, individuals will benefit from its advantageous, some will experience the disadvantages
–> argument doesn’t depend on prior existence of senescene
Alzheimer’s disease
- genes that predispose to Alzheimer’s disease –> selected for because of earlier benefits –> influenced by genetic factors
- genetic changes –> led to very rapid increases in humans brain size
- genes with early benefits contribute to senescene
trade-off
- an evolutionary trade-off, advantageous in early life, contributes to diseases
–> gene involved with big brains, genes that have byproduct of raising risk of Alzheimer’s
enhancers
- pieces of DNA with the ability to boost the activities of certain genes, therefore, levels of resulting proteins
- 93 enhancers expresses within neurons and neuronal stem cells that evolve rapidly in humans
- genes close to these enhancers –> under their control, important for the brain development –> enhancers positively selected for during evolution because of effects of these brain-related genes
- selection diminishes with age because fewer and fewer individuals are around to be selected against –> diminishes rather than disappearing all together
- associations between enhancers and aging-related diseases not definite evidence of cause and effect
menopause
- unlikely to be simply a result of senescene because most common species continue to have reproductive cycles …
- women make substantial effort in each child, investment will pay off genetically
cell genomics
- genetic adaptations to pathogens and increased risk of inflammatory disorders in past-neolithic europe
1. ancient genomic studies allow detection of extent of natural selection overtime
2. genetic adaptation in europe–> occurred at start of bronze age
3. immunity genes –> strongly affected by + and - selection
4. resistance to infection increased inflammatory disease risk
why will selection only very slowly eliminate a fatal, disease-causing, recessive allele from a population
- Hardy-weinberg equation tells you that most copies of the disease-causing alleles exist as heterozygotes
- recessive disease-causing alleles do no harm when heterozygous
- selection only removes fatal disease-causing recessives when they exist as homozygous and homozygous are less common than heterozygous
- as fatal disease-causing alleles diminish in frequency as removed by selection, homozygous of diseases-causing alleles because especially rare, thus only rarely removed by selection
2 components of williams theory of senescene are
- force of selection diminishes with age
- that genes benefit you when young and harm you when old (antagonist pleiotropy) will be favoured by selection
how does figure 8-1 illustrate that “senescence is a first-class evolutionary mystery?”
- individuals who don’t senesce who have much greater reproductive success (indicated by grey area)
