Biology 3&4 Summaries PDF

Experimental method Summary Independent variable/IV: the variable that is being changed in the experiment Dependent variable/DV: the variable that is being measured Controlled variables(s): variables that are kept the same to ensure the validity of the experiment Validity: Measurements measure wha...

Experimental method Summary Independent variable/IV: the variable that is being changed in the experiment Dependent variable/DV: the variable that is being measured Controlled variables(s): variables that are kept the same to ensure the validity of the experiment Validity: Measurements measure what is supposed to be measured, investigates what is supposed to be measured. If measurements are valid, they’re also accurate (see Accuracy). Reliability: How close or consistent the results of repeated experiments are to each other. Data is reliable if the results are the same or approximately the same when the experiment/measurement is repeated. Accuracy: how close the data is to the expected results Systematic errors decrease the accuracy of the experiment: all data results are consistently different from the accurate results. These types of errors can be reduced by controlling more variables and using equipment properly, etc. Example: Selection of wrong equipment, broken equipment, or poorly controlled experimental design, etc. Precision: how close the data results are to each other Random errors decrease the precision of the experiment: unpredictable differences in the data results. These types of errors can be reduced by repetition and averaging. Example: External variables that interfere with the experiment (a noisy classroom when doing a reaction time experiment which requires concentration). Chapter 1 Summary Definitions: Nucleic acid = information molecules which contain information to make proteins Protein/more than one Polypeptide = chemicals in living things that make up man structures and perform many roles/functions (e.g. haemoglobin, keratin, enzymes, hormones, etc.) Proteome = complete array of proteins made by a cell/organism (more complex than the genome because there are way more proteins made than genes) that tells us how a cell works Amino acids: what makes up a protein (monomers of proteins) RNA comes in three forms; mRNA/messenger (transfers DNA code to ribosomes from nucleus), tRNA/transfer (brings specific amino acids to ribosome – codons and anticodons) and rRNA/ribosomal (makes up part of the structure of the ribosome). It’s a single stranded nucleic acid that is composed of 4 bases; A/U and C/G. Similarly, DNA is also a nucleic acid, however it is double-stranded which twists around each other in a spiral, giving it its name ‘double helix’, and the U base which pairs with the A base is replaced with a T base. In its sequence, DNA holds the information to make specific proteins. Depending on the order of the code, different proteins are created. Condensation polymerisation is the joining of two amino acids (polymer). There are four levels of protein structure; primary, secondary, tertiary and quaternary. Primary (polypeptide) – linear sequence of amino acids/monomers. Secondary – alpha helices (coils) and beta-pleated sheets (folding) caused by interactions between R groups. Tertiary – folding of polypeptide (functional) Quaternary – more than one polypeptide (can be a different protein) bonded together Ribosomes are the sites of translation, in which amino acids are joined to form polypeptides. Through its network of channels, the rough endoplasmic reticulum is involved in transporting some of the proteins to various sites within the cell. The golgi apparatus packages proteins into vesicles for export from the cell through exocytosis. 1. Nucleus codes for proteins (makes pre-mRNA) 2. pre-mRNA is capped and tailed making mRNA 3. mRNA exits nucleus and goes to ribosomes in rough ER 4. Ribosome uses mRNA code to make a protein which is folded and modified in ER 5. Transfer vesicle moves to golgi apparatus where it is further modified 6. Protein is packaged into secondary/secretory vesicle for export via exocytosis Protein synthesis consists of two steps; transcription and translation. Transcription – RNA polymerase reads DNA to make mRNA Translation – inside the ribosome, tRNA brings amino acids to attach onto mRNA to make a protein strand Nuclear DNA is ‘unzipped’, read and copied into pre-mRNA by RNA polymerase – an enzyme that makes RNA. Pre-mRNA is modified – methyl cap (5’) and poly-A tail (3’) added and introns removed – to form mRNA (just exons). The mRNA moves to a ribosome (aka rRNA). As mRNA moves through the ribosome it is read in threes (codons). tRNA with an anticodon that matches the codon brings a specific amino acid to the ribosome and adds it (condensation polymerisation) to the polypeptide/protein. Each tRNA carries a different amino acid – all tRNA with the anticodon UAC will carry the met amino acid (START). The trp operon allows prokaryotes to make the amino acid tryptophan when there is none available. When trp is available, the production of it will be stopped through repression or attenuation. Repression is when trp is abundant, it will bind to a repressor protein and activate it. An activated repressor will bind to the operator region of the operon and block RNA polymerase from transcribing the genes. Attenuation doesn’t stop the initiation of transcription like repression. Instead it stops it from being completed, relying on the leading region rather than the repeater. (Abundant – if the ribosome is moving quickly along the leader, a terminator hairpin will form on 3 & 4 making transcription end // Scarce – if the ribosome is moving slowly along the leader, an anti-terminator hairpin will form on 2 & 3, making transcription continue) The genetic code as a universal triplet code that is degenerate (codons produce various amino acids) → different triplets code for the same amino acid. Chapter 2 Summary Endonucleases are restriction enzymes from bacteria that are part of their immune systems. Each restriction enzyme cuts DNA at a specific location/sequence – the recognition site. They can result in blunt or sticky ends. Blunt ends are useful for silencing genes or for electrophoresis, and sticky ends are useful when we want to move or add DNA. Recombinant plasmids are prokaryotic circular DNA that is created by cutting a plasmid with endonuclease for sticky ends in order to add extra DNA. The new DNA is stuck on using DNA ligase. Bacteria share plasmids to share traits. In order to transform bacteria, recombinant plasmids are taken up by bacteria using heat shock (disrupting the stability of the membrane so that it becomes leaky). Bacteria are used nowadays as human insulin factories. Gel electrophoresis is used to separate DNA fragments according to size (base pairs). The end with the wells where the DNA fragments are placed is negatively charged, so the overall negatively charged DNA repels this side and is attracted to the positively charged other end, making the DNA move once a current is added (a saline buffer is added to the gel to help). Larger fragments end up not going as far as small fragments because of the webbing in the agarose gel. DNA polymerase is an enzyme that catalyses the replication of DNA. It is used in polymerase chain reaction – PCR. 1. 90+ – denature/unzip DNA 2. 55 – primers bind 3. 72 – DNA polymerase extends using free nucleotides CRISPR-Cas9 is the immune system of bacterial cells. After infection with a virus, the cell will store a section of the viral DNA in CRISPR. CRISPR is alternating viral DNA (spaces) and palindromic repeats. A section of one repeat and one spacer will form guide RNA (gRNA) that can attach to the Cas9 enzyme and ‘tell’ it where to cut. To avoid cutting the bacteria’s own DNA, Cas9 needs to bind to the non-self region known as PAM. It will then check if the gRNA matches the DNA before cutting. This will kill the virus/silence the gene. Chapter 3/4 Summary Inputs Outputs Photosynthesis (anabolic) is the process that converts sunlight into glucose energy for the plant. But how exactly does this happen? Within the plant, photosynthesis occurs in the plant cells; specifically in the chloroplasts; green coloured organelles in plant cells which are pigmented by chlorophyll. It is the chlorophyll that captures the sunlight energy (red/green light) which energises electrons and protons (H+ and E-) within the chlorophyll, in order to split the water molecules into hydrogen and oxygen (and electrons). The hydrogen then binds to ADP and NADP+ in order to convert them into ATP AND NADPH, while the oxygen is released as gas (as the oxygen gas is released, carbon dioxide is welcomed into the stomata during the day). This process is called the Light Dependent reaction – which occurs in the grana (section of chloroplast that contains chlorophyll); the first stage of photosynthesis. The second stage of photosynthesis – the Light Independent reaction, occurs in the stroma (fluid surrounding grana), and is caused by rubisco; the main enzyme that helps produce glucose. Rubisco helps create glucose by converting the inorganic carbon dioxide molecules (remember that carbon dioxide enters the stomata when the oxygen gas is released?) into organic/solid molecules. This conversion occurs in a process called the Calvin cycle. In the first stage of the cycle, the carbon dioxide molecules use the ATP and NADPH to reconstruct itself into glucose (𝐶𝑂2 ⇒ 𝐶6𝐻12𝑂6 ). When the reconstruction takes place, ATP and NADPH become unloaded again into ADP (+P) and NADP+ and go back to the grana to be recycled. Cellular respiration (catabolic) involves glycolysis, krebs cycle and the electron transport chain (ETC) and can be aerobic, mostly taking place in the mitochondria and is exergonic (releasing energy). 1. Glycolysis – doesn’t need oxygen, occurs in cytoplasm Equation: glucose + 2NAD + 2ADP - 2Pi → pyruvate + 2ATP + 2NAD + 2H+ 2. Krebs cycle – borrows 6O2 from ETC, occurs in matrix Equation: 2 pyruvate + 8NAD + 2ADP + 2Pi + 2FAD → 6 carbon dioxide + 8NADH + 8H + 2ATP + 2FADH2 3. ETC – can’t happen without oxygen, occurs in cristae Equation: 6 oxygen + 10NADH + 2FADH2 + 12H+ → 6 water + 26/28ATP + 14H+ Cellular respiration can also be anaerobic, aka; fermentation. In animals, this results in lactic acid, while in bacteria, this results in ethanol and carbon dioxide. From each glucose, 2ATP is made. Inhibitors can be reversible/weak or irreversible/strong (often poisons). Chapter 5 Summary Definitions: Disease = a condition that interferes with the normal functioning of an organism; usually with specific symptoms Antigen = substances that cause an immune response Pathogens = microbes that cause infectious disease All pathogens act as antigens, but not all antigens are pathogens. (aka, all pathogens cause an immune response but not all antigens are harmful for the body – e.g. self markers/self antigens) Virus = cause disease by killing body cells MHC-I = ‘self’ marker → on all cells MHC-II = present antigens to helper T Complement proteins = inactive enzymes in blood that complement that function of immune cells Interferons = released from virally infected cells to prepare neighbouring cells for a possible ‘attack’. There are three lines of defence in the body’s immune system; the first line, second line and third line of defence. These levels can be split into two types of immunity; innate (non-specific → it attacks all non-self cells) and adaptive (specific → targets certain pathogens). The first two lines of defence involve innate immunity whilst the third line involves adaptive immunity. First line The first line of defence includes a series of physical barriers that prevent pathogens from entering the body. These barriers include enzymes in tears, mucus, eyelashes, nostril hairs, earwax, an acidic skin microbiome, cilia in the lungs, stomach acid, an acidic environment in the reproductive organs, acidic urine, etc. Second line The second line of defence proceeds when a pathogen has broken through the first line of defence. It involves the inclusion of phagocytes such as macrophages and neutrophils, which undergo phagocytosis. Phagocytosis is a process by which: 1. Phagocyte detects a microbe/pathogen and its receptors take it in via endocytosis 2. The microbe is placed in a vesicle 3. A lysosome adds digestive enzymes to the vesicle (fuses) 4. The enzymes break down the microbe 5. The phagocyte expels the debris via exocytosis. The second line of defence also has a process called degranulation. Degranulation is a process by which NK (natural killer) cells recognise an abnormal cell and releases proteases and perforin (which punch holes in the cell membrane for the proteases to enter), so that the cell will undergo apoptosis. NK cells are activated by interferons, which: signal infected cells to undergo apoptosis, uninfected cells to prepare to destroy RNA and reduce protein synthesis, and change the plasma membrane so that making entry for the virus is more difficult. Complement proteins are also part of the second line of defence – as part of the ‘humours’ (involves chemicals and processes). Once activated by making direct contact with molecules on the surface of a pathogen, complement proteins mark pathogens so that other complement proteins may be activated, forming a cascade. This process of marking is called opsonization. Complement proteins can cause inflammation (see below), enhance phagocytosis or cause lysis. Inflammation is the main weapon of the immune system – it prevents the spread of antigens, removes pathogens and dead cells, and restores the tissue to normal. There are 4 stages to inflammation; initiation, vasodilation, migration and resolution. 1. Initiation – damaged cells (mast cells) release histamines and cytokines (and other chemicals). 2. Vasodilation – histamines cause the capillaries to become permeable (leaky/like a sponge) and wider - allows white blood cells and nutrients to move into tissues (symptoms include: redness, swelling, pain). 3. Migration – phagocytes are attracted to the site by cytokines, and phagocytose the antigen and release more cytokines and histamines - complement proteins opsonise the pathogen - platelets travel to the site to block the wound. 4. Resolution – tissue is returned to its original state - the release of cytokines stops and the release of anti-inflammatory cytokines begin. Without resolution, chronic inflammation may occur. Mast cells are also involved in the allergic response. They have granulocytes located near and on the orifices of the body (where there is most likely to be contact with the outside world). To activate mast cells, two steps are required: 1. Sensitisation – initial exposure to the allergen  The allergen enters the bloodstream and APCs (antigen presenting cells) present it to B cells, causing them to differentiate into plasma cells and produce antibodies (IgE) which attach to the mast cells. 2. Allergic reaction – secondary exposure to the same allergen The allergen binds to antibodies on primed mast cells (enough antibodies attach themselves to mast cells over time) which release histamine if enough attach, ensuing an allergic reaction. Third line The third line of defence is where adaptive immunity makes its appearance. This line of defence involves two types of separate immunity as well; cell-mediated and humoral. Cell-mediated immunity is caused by cytotoxic T cells. Phagocytes will present antigens of substances they have phagocytosed on MHC-II markers, acting as antigen-presenting cells (APC). They will travel to the lymph nodes and present to helper T cells and cytotoxic T cells until they find the one with matching receptors. The cytotoxic T cells bind to APC and wait. Helper T cells are activated by APCs. Helper T then search for cytotoxic T with matching receptors and secrete cytokines. Cytotoxic T cells are activated by the binding of APC and the signal from helper T. Activated cytotoxic T cells (clonal selection) will clone themselves (clonal expansion), with some clones becoming memory T cells and some becoming ‘effector’ T cells. Effector cytotoxic T cells find abnormal body cells (by searching for antigen presented on MHC-I) and secrete chemicals to induce apoptosis. Humoral immunity, on the other hand, is when the cytokine signals from the helper T cells, in conjunction with binding to a free-floating antigen, activates a B cell (clonal selection). This causes clonal expansion, where the B cell replicates and some become memory cells while others become plasma cells (see previously: allergic response). Plasma cells make and secrete antibodies which inactivate antigens by clumping, opsonizing, etc. Each antibody is made of 4 polypeptides and has 2 antigen-binding sites. Clonal selection (CS) and clonal expansion (CE) occur in the lymphatic system. The lymphatic system contains lymphocytes such as T and B cells (which mature in the thymus) and lymph fluid (leaky blood vessels + tissue fluid). Lymphatic vessels act as a transparent system for immune system cells. Lymph nodes contain T and B cells and, along with tonsils and the spleen, are where they are activated for CS and CE. MABs can also treat autoimmune disease by; attaching to plasma cells/antibodies, reducing the immune response (less autoantibodies made), etc. Chapter 6 Summary An epidemic becomes a pandemic once it affects more than one WHO region/continent. Factors that contribute to pandemics; 1. New/emerging pathogen appears 2. The new pathogen causes illness 3. It is easily transmitted 4. Uncontrolled spread occurs across a wide geographic area Control measures can include; 1. Quarantine 2. Lockdown 3. Social distancing 4. Mandatory mask usage (infected/symptomatic people) 5. Hygiene – sanitisation Herd Immunity is the theory that mass vaccinating reduces the risk of infection for those who are unvaccinated. Reasons for not undergoing vaccination can include being immunocompromised, undergoing cancer treatment, being/having a baby, being an elder, etc. Vaccines are substances that cause an immune response. They can be live attenuated, inactivated, toxoid or subunit. They help the immune system make its own memory cells against a pathogen. Immunotherapy includes vaccinations, cytokine injections, immune inhibitors and monoclonal antibodies. Monoclonal antibodies (MABs) are antibodies that come in only one shape, which can be designed to target cancer cells and treat autoimmune diseases. They’re created by injecting an animal with an antigen (receptors found mostly on cancer cells, chemicals secreted by cancer cells to allow growth, etc.) to form plasma cells. The plasma cells are extracted and fused with tumour cells to form ‘immortal’ hybridoma cells that can indefinitely make MABs. There are 4 main modes of action of MABs and they are to; stop growth of new blood vessels, signal immune cells to attack, block growth factors, deliver anticancer or radioisotopes to cancer cells. Chapter 7 Summary Definitions: Phenotype = physical or visible characteristics/traits Gene = DNA that codes for protein Allele = variations of a gene (e.g. gene = hair, allele = different colours of hair) Gene pool = population’s various alleles Change to a population’s gene pool is evolution. This can occur through mutations, differential survival/reproduction, migration, random events or human intervention. Mutations can be point [insertion + deletion {frameshift}, substitution] or block (chromosomes) [translocation, insertion, duplication, deletion]. Point mutations; Silent = change in nucleotide does not change amino acid Nonsense = codes for STOP codon Missense = changes one amino acid The four factors that affect allele frequency in gene pools are; 1. Mutation 2. Environmental/natural selection 3. Gene flow/migration 4. Genetic drift/random events/chance factors: founder/bottleneck effect 5. Human intervention (breeding). The Hardy-Weinberg equilibrium is the idea that large populations with random mating and no mutations/natural selection/migration undergo no evolution. Natural selection occurs when any selecting agent acts on a population and causes differences in survival and reproduction of variants (can be for or against). These differences also result in changes to allele frequencies (aka, evolution). E.g. white rabbits survive over brown rabbits in snowy terrain when predators are near as they camouflage better. Selection pressures are external agents which affect an organism's ability to survive in a given environment which can be predator, physical (climate change), biological (competition) or chemical (pollutants). Selection acts on the phenotype and changes the genotype (gene pool – allele frequencies). Evolution theory requirements 1. Organisms produce more organisms than actually survive 2. Every organism must struggle to survive 3. There is variation within a species 4. Some variations allow members of the species to survive and reproduce better than others 5. Organisms that survive and reproduce pass their traits to their offspring and the helpful traits gradually appear more in the population Minimising evolution of resistance in bacteria towards antibiotics 1. Only use antibiotics when needed 2. Use narrow-spectrum antibiotics (specific) 3. Complete the entire course of antibiotics 4. Phage therapy Manipulating gene pools 1. Artificial selection 2. Artificial insemination 3. MOET 4. Sex selection 5. Oestrus syncing Gene flow is one of the things that causes changes to a population’s gene pool; it describes the migration/emigration of organisms. There are also chance factors which affect a gene pool, such as the bottleneck and founder effect, which fall under genetic drift. The bottleneck effect is when the size of a population is radically reduced due to environmental events. Since the size of a population increases variety in the gene pool, it decreases when the size decreases. The founder effect, on the other hand, is when a small amount of organisms splits off from a bigger population and starts a new one, reducing genetic variation. Antigenic Drift is small mutations in RNA that accumulate over time which results in the antigens becoming unrecognisable by memory cells. Antigenic Shift is large changes to RNA that occur quickly which can be brought upon by multiple different viruses combining to form a new subtype. Chapter 8 Summary Definitions: Fossils = preserved remains, impression or trace of a once-living thing from a past geological age (10,000+ y.a.) Mineralised/Petrified Fossil = the organism (hard parts usually) are replaced by minerals Mould Fossil = the impression of the organism is left in rock Cast Fossil = a mould is filled in Trace Fossil = evidence of the organism’s presence e.g. footprint Species = organisms that can produce fertile offspring Index Fossil = useful for dating and correlating the strata in which it was found Adaptive Radiation = rapid speciation of one species into many, each filling a different ecological niche Fossilization 1. Organism dies 2. Rapid burial → prevent scavenging/predators and decomposition 3. Low oxygen/temperature → prevent decomposition 4. Time to turn into rock/fossil (filled with minerals) + undisturbed Determining relatedness Relative dating uses the position (strata) of a fossil to determine its ‘age’ → a fossil in the lower strata is older than one in higher strata. Index fossils (organisms that were widespread for a short time period) can be used to determine the relative age. Absolute dating compares ratios of parent elements (radioactive) to daughter elements using half-life. Half-life is the time for half a parent to decay into the daughter. (C14:N14) Allopatric speciation is the formation of new species due to a geographic barrier. 1. Population has variation 2. Barrier presents gene flow 3. Each population changes due to different selection pressures 4. Over time, each population becomes too different to mate Sympatric speciation Howea palms (Howea b and f) live in the same area and have a recent common ancestor. The ancestor evolved into different species without the presence of a geographic barrier. 1. Variation in the time of flowering in the ancestral population (related to soil) 2. Increased over time, reducing overlap 3. Until some individuals flower only in November and others in December 4. Preventing breeding/gene flow ⛬ different species Evolution of Life 1. The Earth is born (4.5 billion years ago) 2. The origin of life (4-3.5 billion years ago) 3. Life harnesses the power of sunlight (3.4 billion years ago) 4. The first sex (1.2 billion years ago) 5. Multicellular life (1 billion years ago) 6. The Cambrian Explosion (535 million years ago) 7. Plants colonise the land + First insects (465 million years ago) 8. The first mass extinction (460-430 million years ago) 9. Fish that walk on land (375 million years ago) 10. Dawn of the reptiles (320 million years ago) 11. The great dying (252 million years ago) 12. The first mammals (220 million years ago) 13. The Triassic extinction (201 million years ago) 14. The first birds (160 million years ago) 15. Flowers flower (130 million years ago) 16. Death of the dinosaurs (65 million years ago) 17. The first primates evolve (60-55 million years ago) 18. The first hominins (13-7 million years ago) 19. The human race (200,000 years ago) Chapter 9 Summary Determining Relatedness All life is related but we can determine how closely related (how long ago a common ancestor was shared) by comparing DNA or amino acid sequences (molecular homology). As mutations in DNA occur randomly and can accumulate over time, it can be assumed that more differences mean a more distant relationship and fewer differences indicate a more recent common ancestor. Structural morphology Vestigial structures are remnants of structures that were useful in ancestors but no longer have a function (e.g. tailbone). They are evidence of ancestry. Homologous structures are those that derive from a common ancestor but have become different due to different environments/selection pressures (e.g. wings in birds and insects). Chapter 10 Summary Hominin evolution Humans last shared a common ancestor with Chimpanzees about 6 million years ago. We are the last extant hominin species. Mammals → feed milk to young and have fur Primates → grasping hands and binocular vision e.g. monkeys, lemurs, gorillas Hominids → large brain, no tail e.g. apes; gorillas, chimps Hominins are distinguished by being bipedal. Trends in hominin evolution Over time, human skulls have tended to increase in size due to larger brains. Australopithecine species have 300mL brain volume compared to Homo sapiens of 1400mL. Our eyebrow ridge, jaw and teeth have all decreased in size over time. Limb changes: Homo species have longer legs, a broader and shorter pelvis and a less-angled hip bone compared to Australopithecines. These all support more efficient bipedal motion. Human migration We think H.heidelbergensis evolved into H.sapiens and H.neanderthalensis, and that H.erectus evolved into H.heidelbergensis. We know that: H.sapiens migrated worldwide H.erectus migrated to Asia + Europe Two theories on migration exist: Out of Africa proposes that H.sapiens evolved once – in Africa, and then migrated. Multiregional proposes that H.sapiens evolved from H.erectus in Africa, Europe and Asia. mtDNA is useful to determine close relationships because: It does not recombine It has a high mutation rate Specific mutations are assigned to haplogroups Haplogroups show where the mtDNA (the person’s ancestors) evolved. Differences in mtDNA can show the age of populations → more difference = older. Australian mtDNA shows they arrived at least 55000 years ago.