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Lecture 4

ANT208 Lecture 4.rtf

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Department
Anthropology
Course
ANT208H1
Professor
Dan Sellen
Semester
Winter

Description
Anthropology 208 : developmental biology and life histories • Genes • Mutations o Ultimately, the source of new variation** o Produces new genes • Recombinant + assortment o Produces new combination of genes in genomes Both of the above may have NOTHING to do with natural selection!! -some of the forces that produce varation may have NOTHING to do with adaptation -maybe due do only random process, NOT natural selection • Drift, gene flow, mating, bottlenecks, founder effects • Genotype to phenotype • Genomes, proteomes o Think or organisms as clusters as genes that can produce a whole bunch of outcomes for that individuals  The endpoints we arrive at depends on how the genome is translated into the proteome Some of the variations we see are not heritable Only the variations of individual bodies that are heritable can be selected for or against Genes • A chunk of DNA o Contributing to function, phenotype o Is transcribed to RNA then translated into protein • The above is a geneticist’s definition… • Basic coding of bodies • ~>20,000 coding genes in humans o This is only 2% of the DNA in our chromosomes (~6.3-4 billion base pairs) o A lot of NC DNA may have functions that isn’t direct production of proteins o Each of these 20,000 genes can have multiple variations  Some variations may be associated with poor health out comes, some with better health outcomes • Having the gene won’t necessarily mean that you’ll have the disease, the environment plays a role as well • Survives across generations : the unit of natural selection (this is the evolutionist’s definition of a gene) • A gene is immortal until broken up by recombination o If it doesn’t obtain a mutation, it’ll move from body-to-body throughout generations o Passed on through meiosis in the gametes of the body o Potentially the most important piece of the puzzle of natural selection • Genes may not work together in teams • Bodies can be manipulated and change through time as genes come and go thourgh the genome o A protein is translated outside the nucleus of human cells in the cell body that does a job o May fold up and make an enzyme o It is translated from mRNA  The key thing about RNA : it can GET OUT OF THE NUCLEUS, unlike DNA o mRNA is build from a primary transcript RNA, which is built from different sections of DNA o exons in the DNA can be broken up at any time via recombination Rare: single gene -> phenotype o most diseases have no single causal gene, o ex. Obesity, type 2 diabetes, cardiovascular disease o genes don’t cause the disease, but they are only one more risk factor in potential development of the disease o which is why we rather call them risk alleles o cause = MANY RISK ALLELES + environmental factors+developmental factors o epistasis = interaction between genes o basically the control of genetic transcription/translation by other genes o lactase persistence and lactase non persistence (example of epistasis) o correlates positively with the T-allele  a piece of DNA upstream of the exons for the transcription into the lactase enzyme protein structure o affects when lactase non persistence switches on  genotypes: CC = LNP; CT = LP; TT=LNP o the T allele is rarer but more common with those with agricultural history of dairying o we don’t like to characterize lactase persistence as a pathology o not from an evolutionary POV salivary amylase correlates with amylase gene cope numbers o amylase digests stach o we all vary in the amount of amylase in our saliva o also associated with how many copies of the amylase genes o some have more copies than others. More genes = more amylase produced o people with ancestral histories of more starch consumption tend to be shifted upwards in having more gene copies gene x environment interactions o ex. Early close-up work and myopia? o No genetic basis to myopia o One of the theories: if you spend more of your early childhood is that if you spend less time staring at the horizon, there may be a critical period in which a child is exposed to myopia  Hasn’t been proven, but if it is, it is an example of the effect of environment on development o **eyes grow faster than the rest of the skull at 5 years of age o Birthweight o Associated with increased risk of chronic diseases for people of certain genotypes o A measure of our life histories o A very powerful health indicator o Predicts quite a lot of things that may happen to you later in life o Also an indicator of what happened to your mom during pregnancy and pre-natal period o Indicator of early life nutrition o Low bithweight: born early, less nutrition, didn’t rise so well while in the crooker  Were smaller  Have less uptake of nutrients from the mtoher’s placenta  In developing country, was associated with early death  In Canada, associated with certain diseases o ….basis for “fetal origins” hypothesis? = “developmental origins of adult diseases (DOAD)” o Textbook diagram:diference in bone density o Doesn’t vary with genes that have to do with vitamin D synthesis o Those with low birthweight have a risk of osteoporosis o Dominant form: high bone density; recessive form : low bone density  Gene + environment = OUTCOME o Avg birthweight : not much effect o High birthweight:  Gene + environment = produces different risk outcomes later in life o Outcomes : insulin resistance and obesity diagram o Risk of insulin resistance is higher among low and high birthweight  Medium birthweight most resistant to insulin resistance o These 2 diseases have been on the rise quite fast o If as a fetus, you are able to detect your mom is poorly nourished, you may reprogram your metabolic pathways to be a more efficient usesr of energy  However if you were canalized into this configuration based on the in-utero cue of undernutrition, you will have undernutrition configuration for life • These pre-programmed pathways may predispose you to putting on weight and problems with glucose digestions  We can say that modern environments aren’t matched to the in- utero development configurations of metabolic pathways  We can frame this as adaptation OR pathology o Birthweight and neonatal mortality graph o First month death: neonatal mortality o Decreases for babies in normal weight range, rise for big babies and small babies o Across time, although the curves of birthweight distribution remain similar, the rates of th death have dropped  Mostly thanks to the quality of healthcare available these days • However the relationship between birthweight and neonatal mortality remains the same!! Developmental plasticity o A single genotype can produce a range of phenotypes o Developmental influences o Ex. nutrition o Phenotypic variation constrained by genetic and developmental factors o There are constraints on what your genes can do and how much variation your body can produce under different environment o Stabilizing selection o For most biological traits, there are average values which most individuals have o Suggests that extreme values have been selected against in the past o Norm of reaction o A conceptual label for the range of outcomes you cou
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