1 Anthropology 9.09.05 Evolution- non-directional Change through time- no goal Darwin: Upper middle class; theology Loved Natural Science Erasmus- Grandfather MS Beagle- 1831-1836. A boat, for a voyage. Darwin may have been invited to be the captain’s companion. Darwin was allowed to go on the trip. He carried a book by Lyle… Galapagos Islands- off NW coast of Ecuador Finches. He started studying birds. Darwin’s- evolution- descent with modification Progeny (offspring) Darwinian evolution: Simple, elegant Simple: components a. Variation- essential component b. B. Natural selection- pressures that determine: whether or not they will survive Reproduction success Examples of pressures: food source, environment, Obvious pressures: Disease Food supply Climate Predators Less obvious pressures: Territory (Birds, bears, raccoon) Ability to adapt to new territory. Adaptive advantage Reproduce at expense of others Reproductive success- survival of fittest a little misleading.. Whether you leave offspring who survive If your offspring, you are successful in terms of evolution. Why? - variability for continuing change
2 NO MECHANISM TO PREVENT MAXIMUM REPRODUCTION CAPACITY NO GUARD AGAINST EXTINCTION EITHER EXTINCTION ACTUALLY THE RULE LESS THAN .1% OF ALL SPECIES THAT EVER LIVED ARE ALIVE TODAY! Interaction between pre-existing variation and natural selection (reproductive success) promotes non-direction change thru time. Selection operates n variability What will be passed down? Lyles’s influence on Darwin. Malthus’s influence Populations- checks and balances in nature Food supplies cannot keep up with reproduction of populations- doubling can occur ever 25 years. Impulse to multiply- checked b fierce struggle for existence in nature. (Bands of hypoplasia illustrate an interruption in growth and development. Harris lineslittle white bands at the top and the bottom of the tibia. Also known as tranverse lines where the most growth takes place. In his eye organ he has little white holes called cribra orbitalia. Iron core diet.) MALTUS DEMONSTRATED TO DARWIN: SELECTION- operates on individual EVOLUTION- operates on population MEANING: small changes that accumulate and change gene frequency of characteristics eventually change populations. Through time speciation: can change. COMPONENTS OF DARWIN’S THEORY (IN TEXT) 1. Offspring production- faster than food. 2. All living things vary. 3. More born than can survive; fierce struggle. 4. Those with favorable traits survive. 5. Environmental context determines if trait is beneficial. 6. Over long periods- successful variations produce great differences- result- new species. 7. Traits are inherited (passed down). Non-directional change through time is really a change in the gene frequency from one generation to the next. Darwin- did not understand source of change or mechanism. Peppered Moth-England.
3 Moth Story Represent three things: 1) Industrial Melanism Change in gene frequency due to environmental impact 2) Adaptation to environment 3) Natural selection Genetics and Human Variation Genetics is 5-6 billion ppl live on earth today - biological communication between generations - Focus of heredity and variation - Recipe Germ Cells- Gametes Females- ovum (ova) Males- Sperm Zygote- initial cell of offspring Cell- basic to all forms of life Cytology- study of the cell Two kinds of cells involved in heredity 1. Somatic- “soma” 2. Sex cells (gametes) Cell contains: A. Cytoplasm B. Nucleus Nucleus contains: DNA- deoxyribonucleic acid RNA- ribonucleic acid James Watson and Francis Crick 1st Published- 1953 Nobel Prize- 1962 Who else was instrumental to figuring DNA configuration? Rosalind Franklin..died 1958 Nature of cells is to divide Chromosome (Chroma) consists of these things: Arm Centro mere Arm
4 Humans- 46 chromosomes in each somatic cell - 23 pairs Autosomes- 1st 22 pairs Sex chromosomes- 23rd pair
Chimps have 48 chromosomes
Some characteristics on the x isn’t present on the y. DNA and RNA transfer heredity into action DNA- double helix Cell Division: Mitosis- somatic cells 1. Chromosomes double- becomes 92 chromatids still held together by Centro mere. Mitosis continued… 2. Position along equator of nucleus.. single file 3. Move in opposite directions 4. Result- 2 daughter cells identical to original diploid number. 46 chromosomes in each somatic cell. Meiosis- gametes -takes place in gonads Males= testes Females= ovaries - also called Reduction/Division - necessary for bisexual reproduction - Must end up with only 23 chromosomes (haploid) instead of 46 in somatic cells. Mature gamete has how many chromosomes? 23. Sex cell- 23 from one .. 23 from the other…. Steps of Meiosis 1. 2. 3. 4.
Chromosomes double Line up in pairs (instead of sincle file like Mitosis) 1st divison- 23 doubled chromosomes in each cell Line up in single file and divide again – males- 4 cells (gametes) -females- 4 ova but only 1 is viable -polar bodies
Mitosis vs. Meiosis Fertilization occurs- intial cell of the offspring (zygote) Gene- segment of chromosome that codes for a particular protein
5 On chromosome- gene has specific position- locus (address) Thousands, perhaps millions of “loci” Gene at particular locus codes for same heredity characteristic as gene at that location on matching chromosome Homologus pairs- true for first 22 pair (autosomes) 23rd pair (sex chromosomes) are different Y is smaller than the X Male= one X and one Y Female= Two x’s Female can give only an X Male determines sexof offspring From where does variation come?? 1. Mutation (only true source of change of variation 2. During meiosis, doubled chromosomes line up in pairs before first division- line up differently every time they line up. 3. Also- crossing over and recombination4. No two sex cells will be the same. 9/14/05 Remember- nucleus is focal point for heredity In nucleus- DNA and RNA DNA- four bases called nucleic acids Adenine Thymine Guanine Cytosine RNA- four bases Adenine Uracil Guanine Cytosine Note: In TNA you have Uracil rather than Thmine. Base Pairing Rule- certain bases pair (or “bond”) with only cerain other bases: C with G G with C A with T T with A
6 DNA bases combine with sugar and phosphate residues to form “nucleotides” DNA chain composed of nucleotides. Nucleotides composed to phosphate and sugar. Nucleotides linked to other nucleotides on the DNA ladder by hydrogen bonds- long chains of nucleotides When chromosomes are duplicating, what you really see: DNA duplicating DNA strand opens up down middle like zipper Corresponding DNA nucleotides attracted to each side Wander in and bond Result: Two new strands- each with one half of the old Semi- conservative model So, - duplication has taken place- how does information get out of nucleus In steps RNA-RNA nucleotides- also in nucleus RNA takes the chemical codes out the nucleus and into the cytoplasm DNA is template- Cannot, should not leave nucleus Up to RNA to get out of nucleus with instructions to build proteins. How- free RNA nucleotides in nucleus (pretty crowded in there) Particular protein (synthesized), DNA chain opens up at very specific spot. Free RNA nucleotides- attracted to sensing side; temporarily bond to the DNA nucleotides in a specific sequence Information complete, RNA detaches from DNA strand. DNA strand closes up RNA strand can leave the nucleus. RNA is this case is “Messenger” RNA Migrates into cytoplasm (FNA strand same as sense strand) In cytoplasm, “code” which RNA carries is converted into a protein How? Organelles- ribosome’s- move along strand of messenger RNA reading the code Ribosome’s- called “protein factories” Every three bases= “codon” (also called a triplet)- represents one of the 20 amino acids that are building blocks of protein Ex: UUU- Phenylalanine UUA- leucine
7 In comes another kind of RNA which is waiting out in cytoplasm. tRNA (transfer RNA) tRNA carries a cargo- fore and aft Fore- anticodon or complementary code Aft- amino acid tRNA “docks” with ribosome, leaves amino acid Polypeptide chains. Added Note: Ribosome’s multiple readings if need be Once t RNA deposits its cargo(amino acid), it detaches from ribosomal chain. Chemical codes for starting and stopping the formation of proteins. IMPORTANT- the kind of protein created depends solely on the DNA CODEImportant to note: Even small mutations can have dramatic impactEx. Point Mutation Hemoglobin- type of molecule in red blood cells Carries oxygen from lungs to tissue; carbon dioxide from tissue to lungs Hemoglobin made up of protein chains One Type- beta chain 146 amino acids in beta chain (438) (Remember: every three bases equal an amino acid) Mutation can occur in only ONE base to produce sickle cell anemia Blacks; Greek islanders Child- mutate gene from both parents- full brown case If bad (called deleterious), why still present? Only one sickling gene can provide adaptive advantage. Full blown case of sickle cell: Major circulatory problems Destruction of red blood cells Enlarged heart; clogged vessels; bleeding from joints Sickling hemoglobin- substitution at “Point 6” in 438 bases “A” instead of “T” Code: “CAC” instead of “CTC” Wrong amino acid brought in: Valine instead of glutamic acid DNA faithful- will produce replicate of exactly what code says Over and Over again Specifics help us understand
8 Genotype- sum total of all hereditary material from both parents Phenotype- physical express of that information Noted earlier- Phenotypes can be greatly altered by environment Diet Exposure to sun Chemicals Important to remember: What we are is an interaction b/w heredity and…… So what about genetics? Gregor Mendel Austrian monk Loved math Used pea plants as models WHY? Distinguishing characteristics: Color, height, shape of seed, etc. Published in 1866- ignored! Work rediscovered around turn of century. Accomplished two impartant things: Helped to eliminate idea of pangenesis (children- blend of parents) Discovered laws of inheritance Mendel’s 2 “rules” or “laws” 1. Law of segregation- genes occur in pairs; pair members separate during cell formation (meiosis) 2. Law of independent assortment- separation of one pair of genes does not influence the separation of other pairs of genes (member of one pair of chromosomes that enters a sex cell is unrelated to which member- male or femaleof any other pair of chromosomes enters that cell). Mendel- very lucky- characteristics he followed on different chromosomes Mendelian traits- discreet of discontinuous traits- traits that are governed by only one locus. Continuous traits are different- hair color; height (multiple loci) Mendel planted peas- carefully observed
9 Came up with “pure bred” stock- those yellow only produced yellow; those wrinkled only produced wrinkled. Then- he crossed them- green with yellow; smooth with wrinkled; tall with short. Followed through many generations and counted results Result: 1st generation- (1st Filial) all smooth; all yellow all tall 2nd filial- key- traits not lost. Terms: dominant vs. recessive- some traits dominate over others. Not so much “dominance” as effect; a dominant allele affects the expression of a recessive one. Dominant written in upper case (D); recessive lower case (d) Terms: Punnett square- predict combinations of particular traits (dominant vs. recessive) in next generation BB (Homozygous dominant) Bb (heterozygous) Bb (homozygous recessive) Genotypic ratio (on right square) 1:2:1
B- allele- alternative form of gene b- allele- alternative from of gene Phenotypic ratio: 3:1
Mid 1800s- scientists in Mendels’s time did not understand Math was his key; others not viewing things the way he did By 1900’s mendel’s idea were “rediscovered” By 1940s- “population” studies taking place Population Genetics studies So: By 1900’s, scientists knew: 1. Characteristics genetically controlled 2. Characteristics affect an organism’s survival 3. Genes are responsible for mmorphology 4. Frequencies will increase if characteristic is desirable; decrease 5 different modes of mendelian inheritance 1. Autosomal dominant trait 2. Autosomal recessive trait 3. Y- linked 4. X- linked dominant 5. X-linked recessive Population- group of individuals that mate among themselves Subdivision of a species
10 Gene Pool- sum total of all genes (alleles) Hardy- Weinberg- early 1900s- predict gene frequency if present distribution knownABO blood system H-W Equilibrium- no appreciable change in gene frequency- no selection going on 2 prerequisites for equilibrium 1. Infinitely large population 2. Random mating- Beards!! 9/19/05 In humans, social rules determine with whom you mate! In actuality four forces keep population out of H-W Eq. 1. 2. 3. 4.
Gene Flow(migration Random genetic drift Mutation Natural Science
1. Gene Flow- movement of genes b/w populations Increases variability in a group Decreases variability b/w groups Example- Hawaii, Japan 2. Random Genetic Drift- statistical randomness in passage of alleles from one generation to next. Only “lucky” gametes are fertilized. Large populations more accurately reflect true frequency of certain characteristics. Random genetic drift- represents “random” factor in evolution Example- car accident- random happening IN large groups- loss balanced out Small groups- greater impact to gene pool Could produce “founder effect” Example- Pinelop Atoll- coral reef island- south seas typhoon 1775- all but 20 killled Population back up to several thousand
11 High frequency- chromatopsia- rare worldwide (recessive trait- cataracts, shortsightedness) Oral tradition explanation versus reality Mwahuele- chief Isoaphahu- cat god Only certain genes get through- genetic bottleneck Founder Effect Yanomamo (villages split- small gene pool) Universal taboo against incest Inbreeding- promotes expression of deleterious genes- threatens group’s survival 3. Mutation- Mutations are evolutionary important ONLY if they can be passed from one generation to the next. Sickle cell anemia- Hemoglobin beta chain- alleles co dominant HbN/HbN- Homozygous Normal- Malaria HbS/HbS- Homozygous for sickling- very ill probably die HbS/HbN- Heterozygous (one normal allele; one sickling) In areas of world where malaria is prevalent- heterozygous has adaptive advantage Plasmodium (parasite cannot live in sickling homozygous or heterozygous blood) Balanced polymorphism- multiple forms of same gene present in a population at an appreciable rate (usually 5% or more) Mutations (cont’d) In ancient times, mutations at birth were signs of impending wars or famine More than 60 kinds of birth defects recorded on clay tablets from Babylonia Dwarfs often regarded as highly prized curiosities- treated well; dwarf tossing Cyclops- ancient myths Acholdroplastic dwarfism- Dominant mutation If present in the genotype, it will be expressed in the phenotype. Dominant Autosomal Mutation Acondroplastic dwarfism- dominant mutation Normal intelligence; body proportions are not normal Long bones shortened
12 Mutation occurs is one gene in every 10,000 people If present in genotype, it will be expressed N(NA)= NA/N N(N)= N/N NA(NA)= NA/NA NA(N)= NA/N N(NA)= NA/N N(N)= N/N
1 in 2 chance for normal growth 1 in 4 chance for normal growth
Problems with some mutations- don’t show up at birth Huntington’s chorea- dominant mutation- onset- during young adulthood- often after childbearing years have already started Dominant mutation Neurological condition- nerve Marfan’s syndrome- Abe Lincoln Sex-linked mutations: Carried on X and not on Y If recessive, takes a double dose for female; recessive or dominant in male, he gets it. Whatever mother is carrying: hemophiliaEX. Queen Victoria carried hemphilia- Passed to many royal families in Europe especially Alexandria marries Czar Nicholas II- Russia- several children Alexis- hemophilia- very ill Alexandria influenced by Rasputin- in turn, influenced Czar Russian Revolution- 1917 Royal Family murdered in 1918 In 1980’s- Anna Anderson- Anastasia? Royal family Exhumed Dr. Williams Maples- Forensic Anthropologist DNA
13 Problems with mutations in predicting some of them is that they can be hidden in the heterozygous individual. Can some kinds of mutation be predicted in future generations? Hiroshima Rad- absorbed radiation change 20-25- break a chromosome Average lethal- 50 rads Chest x-ray- .003 rad; cosmic radiation- 1/20 per year Ground radiation- 1/12 rad per year Hiroshima survivors-200 rads; prediction- 1 lethal mutation Per offspring- has not happened. 4. Natural Selection: those forces that operate on an individual that determines survival Sickle Cell ABO Blood Group: Antigen Systems (ABO,Rh, others) – ABO- blood type Antigen- macromolecules in red blood cells For our purposes, like soildiers who create antibodies Reactions to forerign invasions ABO system If parents give two A’s, child is A If parents give two B’s, child is B If parents give 1A, 1B- child is AB If parents give 1A, 1O- child is A If parents give 1B, 1O- child is B If parents give 2 O’s- child is O “O” is recessive, “O” simple means lack of agglutinating protein Agglutination discovered around turn of 19th century when trying to do blood transfusions- if blood transfusions- if blood not compatible, persons can die. A cannot receive B B cannot
10.3.2005. Ageing and sexing- best bone is the hip bone Auricular- changes throughout our lifetime Sacrum
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Hipbone Pubic bone-changes just like the auricular surface. . Sciatic notch assist in sexing male has narrow notch (acute angle), Female has wider(90 degree angle) notch. Sub pubic angle much broader in a male than a female. Males in general are larger. Females generally smaller than males. The skull helps determine sex… Male square chin, supra orbital tourus , sloping forhead, blunt border on the ear orbit.. large Female- pointed chin, smooth forehead, sharper border on the eye orbit Race: Use the skull for that. Whites- dropeed eye orbital, narrow nasal area, staraighter face Blacks- square eye orbitals, more prominent region Asians- intermediate b/t the too. Dental records help identify someone Positive ID using one tooth. Perimortem- happens during time of death Post mortem trauma- happens after death Blunt force trauma to the head.. makes it all messy Post mortem interval-