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ANS 2: Week 8 Notes

by: Mackenzie Hayes

ANS 2: Week 8 Notes ANS 002

Mackenzie Hayes

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These notes cover everything from lecture including diagrams and lecture slides
Introductory Animal Science
Dr. James Murray
Class Notes
animal, Science
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This 13 page Class Notes was uploaded by Mackenzie Hayes on Sunday May 22, 2016. The Class Notes belongs to ANS 002 at University of California - Davis taught by Dr. James Murray in Spring 2016. Since its upload, it has received 10 views. For similar materials see Introductory Animal Science in Animal Science at University of California - Davis.


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Date Created: 05/22/16
ANS 2: Week 8 Notes (5/16) ● Definitions: ○ Self​ vs.Non-Self: every individual makes self-identification molecules ■ These train your immune system what to recognize as “self” during fetal development, everything else is “non-self” or foreign ○ Antigen​ : ananti​ody-generator ■ Induces immune response ■ Usually non-self origin, pathogenic or not ■ Protein, carbohydrate (less often lipi, DNa, RNA) ○ Epitope​ : a facet of an antigen ■ Each antigen can have several epitopes ■ Each epitope can generate a unique antibody ● Primary and Secondary lymphoid organs ○ Bone marrow: ■ Site of all immune progenitor cells ■ Site of B-cell maturation ○ Thymus: ■ Site of T cell maturation ● Broad functions of immune system: ○ Distinguish self from non-self molecules known as antigens ○ Permit absorption of nutrients ○ Protect sterile environments ○ Mobilize cells to sites of infection/inflammation ○ Contain infection ○ Develop antigen-specific antibodies and long-lasting immunity ■ “Immunological memory” ■ Each B cell is only making one antibody to go against one thing ● Need a whole repertoire of antibodies ● Innate immunity or Nonspecific barriers against pathogens: ○ Nonspecific barriers of the body against invaders ○ Physical barriers: ■ Unbroken skin, mucus, peristalsis, flushing (tears, saliva, urine), cilia ○ Chemicals: ■ Acidic pH (stomach, vagina), sweat, bile salts, digestive enzymes, nonspecific IgA, antimicrobial peptides ● Paneth cells in intestines make defensins, cathelicidins, etc. ● Lysozyme in tears, saliva, milk ○ Microbial: ■ Competition for space for nutrients ● Good bacteria fills the niches that bad microbes would want to take but can’t because it’s occupied ● Passive Immunity: ○ Transfer of maternal antibodies to fetus across placenta ■ Not true in all species ○ Colostrum contains antibodies ■ Antibodies absorbed into bloodstream before gut closure ● <48 hrs postpartum ● After that they are absorbed like any other amino acid ○ Only lasts a few months ○ Milk contains antibodies and antimicrobials ■ Act on microbes at epithelial surfaces ■ Protect against respiratory and GI infection ■ Works as long as milk is being consumed ● What happens?​ If exposed to a pathogen ○ Fever, redness, swelling, pain, decreased function ○ Lactoferrin = most abundant protein in human milk ■ Actively modulates inflammation ■ Ex: Eating food contaminated with pathogenic E. Coli ● Breach of physical and chemical barriers ● Pathogen or toxins make contact with epithelial cells ● Innate Immunity: ○ Once contact is made, inflammation begins ■ Pathogens have common cell-surface antigens ● Pathogen associated molecular patterns (PAMPs) ○ Ex: lipopolysaccharides ● PAMPs bind to epithelial cells ● Resident cells recruit more immune cells ■ Diarrhea in response to inflammation ● Flush out the pathogen ● Leukocytes respond to inflammation ○ White blood cells ■ neutrophils, monocytes/macrophages, Dendritic Cells, Natural Killer Cells ■ Increase White blood cells producition in bone marrow ■ Migrate to site of inflammation ■ Phagocytosis of dead cells and pathogens ■ MO, DC, and B cells are professional antigen presenting cells (APCs) ● When innate immunity fails: Adaptive immune response ○ MO, DC< migrate to Peyer’s patches and lymph nodes ○ T cells bind antigens ○ T cells activated ● T cells activate B cells in PP/LN ○ Helper T cells (Th cells) ■ Provide help to B cells that is necessary for antibody production ○ B cells bind antigen through B cell receptor ○ T cell activates B cells to proliferate and differentiate into antibody-secreting cells ○ Antibodies coat pathogen, targets them for destruction ● When infection is controlled: ○ Must stop immune response ■ Arthritis - your cells are attacking your own body ○ Regulatory T cells suppress inflammation ○ Memory T and B cells form ○ Lasting immunity against pathogen ■ THIS IS HOW VACCINES WORK (5/18) ● Failure of immune system ○ Breakdown of tolerance ■ Autoimmunity​ - identifying self antigens as foreign ● Multiple sclerosis​(attack Central Nervous System) ● Lupus​ (attack various organs) ● Type 1 Diabetes​ (attack beta cells in pancreas) ■ Inappropriate response to non-pathogens: ● Commensal bacteria: Crohn’s and colitis ● Non-infectious antigens: allergies to pollen / food ○ Every surface of your body is colonized by commensal microbes ○ Fine balance between ■ Recognizing antigens from non-threatening sources ■ Distinguishing between commensal bacteria (tolerated) and pathogens ■ speed, strength, and duration of immune response ● Immune cells - originate in bone ● Genetics Definitions: ○ Cell cycle ○ *** ● Genetic Revolution ○ Gregor Mendel - basic mechanisms of inheritance ○ Charles Darwin - genetic makeup over time is plastic (changeable) ■ Every animal differs by thousands of base pairs ● Except clones and twins (closer in genetic makeup) ● Basics: ○ Cell nucleus containschromosomes ■ 3 genomes - mom, dad, mitochondria (from mom) ○ Chromosomes are ​ macro-molecules ■ Contain nucleic acid polymers, proteins, etc ■ large clusters of variety of molecules ○ Genes​ - functional segments on chromosomes ■ Encode specific RNA’s or amino acid sequences (proteins) ■ By way of transcription through RNA ○ Genome - ​ Sum of all genetic material in one complete set of chromosomes ■ 2-3% of your DNA codes for protein ■ Sperm and egg are the only one cells that have a full genome ○ Locus​ - site or location on a chromosome ■ Identifiable ■ Changes between species chromosomes can be used as markers ○ Gene - ​functional region at a locus ■ May or may not code for a protein ○ Alleles -​different versions of a gene ■ Can be many different alleles for a locus in a population ■ Only 2 alleles for a locus in a population ● Compatibility Complex - makes antibodies ○ Clustered around one portion​ of the chromosomes ○ Rest of genes are scattered all over every chromosome of the genome ● Genotype - genetic constitution of an INDIVIDUAL ○ Gametes carry only one allele for every given locus ○ Individuals carry 2 alleles for each autosomal locus ○ Combination of all allele pairs of all gene loci = the genotype ○ Complete genotypes are not inherited ■ We get half from each parent ● Mammals and birds have diploid genomes (2N) ○ Otherwise is lethal ○ Gametes are haploid ○ Fish may be 2n, 4n, or other variations (and amphibians ■ Sturgeon = 2n = 217 +/- 6 ● 2 Types of chromosomes ○ Autosomes:​ paired, diploid organisms, pair at meiosis ○ Sex Chromosomes:​ different between the sexes ■ ZW birds (female) ■ Y/X mammals (male/female) ● Gender is determined by temperature​ (environment) (not chromosomes) ○ In green sea turtles and alligators ○ In humans:​ female development is the default ■ Y chromosome stops that development ● Mitosis​: duplicated DNA and getting ready for dividing (4C) ● Cell cycle​- replication of DNA and duplication of cells mitotically ○ G - ​ap between phases (only place where the process can “pause”) ■ 0 - same as gap 1 but referred to 0 if it probably will never divide again (neurons are in G0) ■ 1 - between division and beginning of replication of DNA ● Can last minutes to hours to forever (variable) ■ 2 - between end of replication of DNA and mitosis ● Also variable amounts of time ● Mitosis - go through cell cycle and chromosomes duplicate ● Meiosis - modification of mitosis ○ 1 - elongated prophase ■ chromosomes pair and crossover (exchange material) ○ 2 - go into divisions with absence of duplicating DNA ○ Results in haploid cells not diploid (5/20) ● Phenotype:​ the observable properties of an organism: ○ Weight, height, milk yield, color etc. ○ (P) results from action of the genetic (G) makeup of an organism, its environment (E), and the interaction between the genes and the environment (GXE) ○ P = G + E + (GXE) ● Eukaryotes vs. Prokaryotes ○ Eukaryotes have ​introns​- breaks up genes = more opportunity for variation ● Meiosis: ○ Meiosis = key to understanding genetics ○ Creates haplous 1N gametes that contain only 1 allele per gene ○ Mendelian inheritance​ is simply following alleles thru meiosis ○ 2 Processes that cause re-shuffling of genes: ■ Random migration of individual chromosomes into gametes ● Results in mix of paternal/maternal chromosomes in each gamete ■ Crossing over / exchange of gene segments btwn homologous chromosomes in prophase of Meiosis 1 ○ No two individuals are identical ■ Every chromosome has to have at least one crossover per meiosis ● Types of Gene Action: ○ Dominant​ : heterozygote has the same phenotype as homozygous dominant (Aa = AA) ■ Action of recessive allele completely masked by dominant ○ Co-dominance:​ Aa =/= AA ■ Effect of both alleles observed ■ Phenotype of heterozygote different from both homozygotes ○ Semi / Incomplete Dominance:​ AA =/= Aa ■ Phenotype of heterozygote is midway btwn that of both homozygotes ○ Epistasis:interaction between genes of different loci ● Coat color in horses ○ Base Coat Color = Dominant ○ The E​ xtension Locus ■ E allele produces both black (eumelanin) and red (phaeomelanin) ■ e allele produces only red pigment ■ EE/Ee = horses with both red and black color (blacks and bays) ■ ee = only red horses (chestnut) ○ Having black points is the same gene as the agouti in mice ● Incomplete Dominance in Horses: ○ Chestnut vs. Palomino ○ C’ = cream dilution allele ○ eeCC = chestnut (dark brown body) ○ eeCC’ = palomino (white points and light brown body) ○ eeC’C’ = cremello horse (all white) ● Epistasis in Horses: ○ G = Grey vs. Extension ○ G masks all other coat colors except dominant white (which trumps all) ○ ggEE/ggEe = black or bay | ggee = chestnut ○ G_ _ _ (anything) = grey ○ All grey horses get melanomas if they live long enough ● Predicting ratios: Single Gene ○ Punnett Square ○ Genotypic Ratio will differ from Phenotypic ○ What goes into each gamete = total chance ○ No 2 individuals have exact same genotype unless clones or identical twins ■ As the number of pairs increases, the number of genotypes grows ● Gene Frequencies ○ INDIVIDUAL can only have 2 alleles at a locus ■ POPULATION can have many different alleles at a locus ○ Count frequency of alleles for a population ■ Corollary​ = allele frequency data is population specific ■ Frequencies change based on: ● Population size ○ If small, one little change in allele can lead to huge change in frequency in population ● Differences in fertility / viability ● Migration and mutation ● Mating system ● Hardy-Weinberg Equilibrium: ○ Assumes: Large population, no effect on fertility, equal viability of all gametes, no migration, no mutation, Panmixis (equal opportunity for all mating possibilities) ○ p​ 2+ 2pq + q​= 1 (p/q each represent an allele) ■ Displays the allele frequency of “next generation” ■ Homozygotes = p​ 2/q​ ■ Heterozygotes = 2pq


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