Bio Exam Revision

secondary structure

the interactions between amino acids cause the natural local bending and twisting of the polypeptide. this includes alpha-helices, beta-pleated sheets, and random coils

messenger RNA

it carries a copy of the genetic code from the DNA in the nucleus to the ribosome

transfer RNA

it carries amino acids from the cytoplasm to the ribosome, and pairs with the complementary codons on mRNA

ribosomal RNA

it makes up about 60% of the structure of ribosomes (the other 40% is protein)

universal

the genetic code is the same in all organisms

unambiguous

each codon specifies only one amino acid

degenerate

most amino acids can be specified by more than one codon

promoter

an upstream binding site for RNA polymerase and other transcription factors. when RNA polymerase binds to the promoter region of a gene, it allows for the transcription of that particular gene

operator

it serves as the binding site for repressor proteins, which can then inhibit gene expression. this region is typically only found in prokaryotic genes, as eukaryotes have different regions for regulating gene expression

leader region

the section of DNA just upstream of the coding region, and downstream of the promoter and operator. this region plays a critical role in one mode of regulating gene expression in prokaryotes

transcription

1. Initiation: transcription factors and RNA polymerase bind to the promoter region, signalling for weak hydrogen bonds between the 2 strands of DNA to break, causing the DNA helix to unwind

2. Elongation: RNA polymerase runs along the template strand in a 3’ to 5’ direction, building a complementary strand of mRNA (pre-mRNA in eukaryotes) in a 5’ to 3’ direction

3. Termination: RNA polymerase reaches the termination sequence, signalling for the end of transcription. RNA polymerase then detaches, releasing the mRNA or pre-mRNA molecule, and the DNA strands anneal

translation

1. initiation: mRNA binds to a ribosome, 5’ end first. the mRNA is read until the start codon (AUG) is recognized. then, a tRNA molecule with the anticodon UAC binds to the ribosome and delivers the amino acid methionine.

2. elongation: the mRNA is fed through the ribosome, matching codons with complementary anticodons. Then, tRNA molecules deliver specific amino acids to the ribosome, which bind to adjacent amino acids with a peptide bond via a condensation reaction

3. termination: the ribosome stops when it reaches a STOP codon, signalling for the end of translation. the polypeptide is then released by the ribosome into the cytosol or rough ER

purpose of gene regulation

to save energy

role of structural genes

they’re responsible for producing proteins that are involved in the structure or function of a cell

role of a regulatory gene

they’re responsible for the production of regulatory proteins such as repressor proteins or activator proteins

Trp operon repression when tryptophan levels are high

tryptophan binds to the repressor protein which induces a conformational change in the repressor protein, changing it into its active form. this allows the repressor to bind to the operator region, preventing transcription by blocking the path of RNA polymerase, inhibiting unnecessary production of tryptophan

Trp operon repression when tryptophan levels are low

the repressor protein becomes inactive and detaches from the operator region, allowing RNA polymerase to transcribe the trp structural genes so tryptophan levels can increase

Trp operon attenuation when tryptophan is present

a ribosome begins translation and runs past the tryptophan codons since there’s enough tRNA bound tryptophan, stopping at the stop codon. this causes the formation of a terminator hairpin loop, putting tension on the attenuator and causing the mRNA strand to pull away from the DNA, detaching RNA polymerase, ending transcription

Trp operon attenuation when tryptophan is absent

the ribosome begins translation, and when it reaches the 2 tryptophan codons, it pauses due to an absence of tRNA bound tryptophan. this allows the formation of an anti-terminator hairpin loop, but because it’s far enough away from the attenuator, the mRNA strand does not pull away from the DNA. this means that RNA polymerase can continue transcription, and a new ribosome attaches to the mRNA strand after the hairpin loop to continue translation

function of the rough endoplasmic reticulum in the protein secretory pathway

if a protein is destined to be secreted, the ribosome synthesising it is usually attached to the rough ER. the environment inside the rough ER allows for the correct folding of the newly formed polypeptide chain before being passed to the golgi apparatus. within the rough ER, polypeptide chains move through the channel network of lumen

role of the transport vesicle in the protein secretory pathway

a transport vesicle containing the protein buds off the rough ER and travels to the golgi apparatus. the vesicle fuses with the golgi membrane and releases the protein in its lumen

role of the golgi apparatus in the protein secretory pathway

proteins are delivered by transport vesicles to the cis side of the golgi apparatus, and as they move through, they’re modified by resident enzymes. different modifications take place in the cis, medial, and trans compartments. these modifications are necessary to target the proteins in their intended destination

role of the secretory vesicle in the protein secretory pathway

secretory vesicles containing proteins for export bud off the golgi apparatus from the trans face and travel through the cytoplasm, fusing with the plasma membrane. this releases the proteins contained from within, into the extracellular environment through the process of exocytosis

purpose of PCR

to amplify DNA, making millions of copies of a small length of DNA in a short amount of time

steps of PCR

Denaturation – DNA is heated to approximately 90–95 °C to break the hydrogen bonds between the bases and separate the strands

Annealing – the single-stranded DNA is cooled to approximately 50–55 °C to allow the primers to bind to complementary sequences on the single-stranded DNA.

Elongation – the DNA is heated to 72 °C, Taq polymerase’s optimal temperature. Taq polymerase binds to the primer, and begins synthesising a new complementary strand of DNA.

The cycle (steps 1–3) is repeated multiple times to create more copies of DNA.

location of photosynthesis

chloroplasts

location of the light dependent stage

grana, on thylakoid membranes

location of the light independent stage

stroma

balanced equation for photosynthesis

6CO₂ + 12H₂O → C₆H₁₂O₆ + 6H₂O

inputs of the light dependent stage

12H₂O, 12NADP⁺, 18 ADP + P_i

outputs of the light dependent stage

6O₂, 12NADPH, 18ATP

inputs of the light independent stage

6CO₂, 12NADPH, 18ATP

outputs of the light independent stage

C₆H₁₂O₆, 6H₂O, 12NADP⁺, 18 ADP+P_i

photorespiration

when it is hot, rubisco can use O₂ as a substrate as well as CO₂, disrupting the Calvin Cycle. this is because rubsico acts as an oxygenase as well as a carboxylase

process of photosynthesis in C4 plants

In mesophyll cells, there’s little to no rubsico. instead, an enzyme called PEP carboxylase takes a CO₂ molecule and combines it with a 3-carbon molecule called PEP, joining them together to form a 4-carbon molecule called malate. malate can go through plasmodesmata tubes into the bundle sheath cell, where it’s broken down into CO₂ and pyruvate. the pyruvate goes back through the plasmodesmata and becomes PEP again, but the CO₂ goes into the Calvin Cycle and gets used by rubisco to make glucose

process of photosynthesis in CAM plants

at night, CAM plants open their stomata to allow CO₂ into the leaf because it’s cooler and they won’t lose as much water. then PEP carboxylase combines the CO₂ with PEP to produce malate. the malic acid then goes into the large vacuole and is stored there until morning. When it gets to morning, the stomata close, and the malate is broken down into CO₂, which rubisco uses to produce glucose. the 3-carbon molecule is then recycled back into PEP so that the next night the process can repeat

adaptation of C4 plants

prevents photorespiration

adaptation of CAM plants

reduces water loss

role of rubisco

rubisco binds CO₂ and fixes the carbon dioxide molecule into the organic 3-PGA, initiating the Calvin Cycle

alcohol fermentation in yeasts

an anaerobic respiration process where glucose turned into ethanol and CO₂. this process occurs in yeasts and some bacteria, enabling them to produce energy in the absence of oxygen. glycolysis occurs as normal then ethanol fermentation. this process occurs in the cytosol

lactic acid fermentation

a type of anaerobic respiration in animals where glucose is converted into lactic acid. this process provides energy when oxygen levels are low. glycolysis occurs as normal and then lactic acid fermentation occurs. both processes occur in the cytosol

applications of anaerobic fermentation of biomass for biofuel production

• fermentation of sugars can yield ethanol

• biodiesel is usually produced from vegetable oils, made by the esterification of the oil, which involves reacting oil with an alcohol in the presence of a catalyst

• bioethanol can be used in almost pure form, but is often mixed with other fuels as an additive

location of glycolysis

cytosol

location of the krebs cycle

matrix

location of the electron transport chain

cristae

overall equation of aerobic cellular respiration

C₆H₁₂O₆ + 6O₂ → 6CO₂ + 6H₂O

overall ATP production during aerobic cellular respiration

30 or 32 ATP

inputs of glycolysis

glucose, 2NAD⁺, 2(ADP + P_i)

outputs of glycolysis

2 pyruvate, 2ATP, 2NADH

inputs of the krebs cycle

2 pyruvate, 8NAD⁺, 2(ADP + P_i), 2FAD

outputs of the krebs cycle

6CO₂, 8(NADH + H⁺), 2ATP, 2FADH₂

inputs of the electron transport chain

26 or 28 ADP + P_i, 10NADH, FADH₂, 6O₂

outputs of the electron transport chain

26 or 28 ATP, 10NAD⁺, 2FAD, 6H₂O

competitive inhibition

occurs when an inhibitor molecule binds to an enzyme’s active site. this binding directly occupies and blocks the active site, meaning the substrate is now unable to bind with the enzyme and no reaction will occur. It’s said to be ‘competitive’ because the substrate and inhibitor are competing for the active site

non-competitive inhibition

occurs when an inhibitor binds to an enzyme at a site other than the active site. this binding causes a conformational change in the active site of the enzyme. the conformational change in the active site’s structure prevents the substrate from binding to it, preventing the reaction from occurring

potential applications of CRISPR-Cas9 to improve photosynthetic efficiency

• engineer crops that bypass photorespiration, somewhat mimicking the function of C4 and CAM plants

• target stomata to reduce the impacts of water stress

• target rubisco’s function directly

antigen

a molecule that promotes an immune response

MHC (Major Histocompatibility Complex) Markers

a group of proteins present on the surface of all self-cells that enables the immune system to distinguish it from non-self material

pathogen

the causative agent of an infectious disease

pathogenic bacteria

unicellular, prokaryotic, organisms that usually produce endotoxins or exotoxins. these toxins affect functioning of cells or cause their death. they typically reproduce asexually through binary fission

fungi

eukaryotic organisms that can be unicellular or multicellular. they contain long, branching filaments called hyphae. they reproduce via asexual and sexual reproduction called spore formation

worms

multicellular, invertebrate parasites. development includes egg, larval, and adult stages. they reproduce sexually

protozoa

single-celled eukaryotes that can be free-living or parasitic. they have many different mechanisms of action. they reproduce through both sexual and asexual reproduction

viruses

non-living infectious agents composed of genetic material inside a protein capsid. they cannot reproduce independently, instead, they insert their genetic material into a host’s cell and use the cell’s machinery to replicate

prions

abnormally folded proteins that can only effect neural structures in mammals. they are the only known infectious agents that don’t contain nucleic acids. they induce misfolding in nearby proteins, therefore spreading throughout a tissue

mast cells

leucocytes that embed themselves in connective tissues. when they detect damage to the surrounding cells, they release histamines that have 3 effects, which are referred to as the inflammatory response

phagocytes

cells that engage in phagocytosis, a process where they consume and destroy foreign or dead material present in the body by engulfing it through endocytosis. once engulfed, lysosomes containing lysozymes present in the cell destroy the foreign or dead material by fusing with the vesicles containing the engulfed material.

reliable

describes an experiment, tool, or measurement that produces similar results when repeated and reproduced

repeatable

an experiment/measurement in which scientists can use the method they designed and obtain the same result multiple times

reproducible

an experiment/measurement in which a group of scientists, using methods designed by others, can obtain the same results as another group’s experiment

valid

a measurement or experiment that actually tests what it claims to be testing

replication

the process of running your test/experiment multiple times

true value

the value that would be obtained by a perfect measurement without the influence of errors

representative

a sample that accurately reflects the characteristics of the larger population

anecdote

evidence involving a personal account or report of a previous experience that may provide a certain level of support for a position

correlation

when there is a relationship between two variables

causation

when change in one variable leads to reliable change in another

metathinking

the practice of reflecting upon and evaluating the way we think, including the different strategies and tools for problem–solving and learning

natural killer (NK) cells

large, granular lymphocytes. they are important in destroying self-cells that have been infected by a virus, or which have become cancerous. On finding a self-cell displaying non-self antigens on its surface, they release a death ligand, signalling the cell to die via apoptosis

eosinophils

large, granulated cells which contain various toxic chemical mediators that help destroy pathogens. they typically target pathogens too large to be phagocytosed by degranulating on contact with them and releasing those chemical mediators contained with their granules

interferons (INF)

signalling molecules (cytokines) released from virus-infected host cells that cause nearby cells to heighten their antivirus defences. cells stimulated by these molecules produce various enzymes that inhibit protein synthesis. they also cause cells to upregulate the production of MHC 1 markers

complement system

a small suite of proteins called complement proteins that are synthesised by the liver, and circulate in the blood in an inactivated state. when activated, they achieve 3 primary outcomes; oponisation (sticking on the surface of pathogens so cells of the immune system can recognise them as foreign), chemotaxis (gathering near a pathogen to attract phagocytes), and lysis (forming a membrane attack complex to create pores in the membrane of a pathogen, causing lysis which makes the pathogen burst)

fever

a complex series of responses can temporarily raise the set temperature pt. of the body during a fever, meaning the body will initiate a no. of countermeasures to increase the core body temp to reach this new setpoint. this is an innate response to potential infection, as many pathogens cannot survive at the elevated temps created. however, when prolonged, it can be detrimental to our body due to the additional stress placed on our cells

inflammatory response

1. Initiation: when pathogens break through the 1st line of defence, macrophages situated in the tissue where the pathogens were introduced become activated, and long with damaged cells, release cytokines. mast cells will also degranulate, releasing histamine

2. Vasodilation: histamines bind to receptors on nearby blood vessels, causing vasodilation. this increases blood flow to the injury site, causing swelling, redness, and warmth. gaps in vessel walls also form, increasing permeability to immune cells

3. Migration: vasodilation allows components of the 2nd line of defence to reach the injury site including phagocytes, which are guided by cytokines. the response continues until the area is cleared and healed

antigen presentation

antigen-presenting cells engulf pathogens via phagocytosis, displaying the pathogenic antigens on their MHC Class II markers. they then travel to lymph nodes to present the foreign antigens, interacting with the complementary receptors on the surface of T helper cells, and activating the T helper cell. the selected T helper cell can then help initiate the adaptive immune response through the humoral or cell-mediated immune response

cell-mediated immune response

Targets infected/abnormal cells. Steps are:

1. clonal selection: antigen-presenting cells find a naive T cell with a matching receptor. T helper cells then release cyotkines, activating the T cell to multiply and differentiate

2. Differentiation: the T cell clones then become: cytotoxic T cells, which travel to the infection site to kill infected cells, and T memory cells, which stay in the body to provide long-term immunity

3. Destruction: cytotoxic T cells bind to infected cells showing the antigen on MHC Class I markers. They release perforin and other chemicals to trigger apoptosis.

4. For viral infections, B cells also produce antibodies, to combat viruses travelling between cells

humoral immune response

targets extracellular pathogens. key steps:

1. Clonal selection: a B cell with a matching receptor binds to a pathogen’s antigen

2. Clonal expansion: A T helper cell releases cytokines, causing the B cell to multiply

3. Differentiation: the B cell clones differentiate into plasma cells and B memory cells

4. Response: plasma cells secrete antibodies to fight infection, B memory cells stay in the body for long-term immunity

antibodies

proteins with quaternary structure that interact with pathogens in a number of ways:

• neutralisation: blocking the active site of pathogens and toxins

• agglutination: binding with antigens on 2 separate pathogens, forming large antigen-antibody complexes, making it easier for phagocytes to recognise them as foreign and destroy them

• immobilisation: restricting the movement of pathogens via large antigen-antibody complexes

• oponisation: binding directly to the surface of a pathogen to make it easier to phagocytose

• activation of complement proteins: antibodies attached to the surface of pathogens can facilitate the actions of complement proteins, including the formation of MACs

B and T memory cells contribution to immunological memory

B memory cells: they rapidly divide and form new plasma cells when they encounter a complementary antigen. they also constantly secrete low amounts of their antibody

T memory cells: they rapidly proliferate into T helper cells and cytotoxic T cells upon stimulation by a complementary antigen to their receptors

primary lymphoid tissues

where lymphocytes are formed and mature. it includes the thymus and bone marrow. all lymphocytes are formed in the bone marrow of long bones, but T lymphocytes leave the bone marrow and mature in the thymus gland

secondary lymphoid tissues

lymph nodes, tonsils, spleen, Peyer’s patches in the small intestine, and mucosal surfaces

lymph nodes

a small secondary lymphoid tissue where antigen-presenting cells activate the adaptive immune response. they act as filters for the lymph flowing back towards the heart. they contain a high concentration of lymphocytes

natural vs. artificial immunity

natural immunity results from an unintentional exposure from an antigen, whereas artificial immunity results from some sort of medical intervention

active vs. passive immunity

active immunity is obtained when a person’s own immune system produces the antibodies, whereas passive immunity occurs when a person has antibodies that were produced by someone else’s immune system

whole pathogen vaccines

vaccines that contain whole pathogens. they include inactivated vaccines (vaccines that contain whole bacteria/viruses that have been killed/altered so they can’t reproduce), and live attenuated vaccines (vaccines that contain whole pathogens that have been weakened through genetic modification or other means)

subunit vaccines

vaccines that contain antigens from a pathogen. they include recombinant protein vaccines (vaccines made by genetically modifying harmless yeast/bacteria so they produce a surface protein of a pathogen), toxoid vaccines (vaccines containing an inactivated version of a toxin produced by a pathogen), virus-like particles (vaccines that contain viruses that have no genetic material), and outer membrane vesicles (vaccines naturally produced by bacteria and are a bleb of the bacterial outer cell membrane)

nucleic acid vaccines

vaccines that provide genetic instructions for making the protein antigen. they include RNA vaccines (vaccines that use RNA in a lipid membrane, which is translated to make the protein), DNA vaccines (aren’t in use but are being developed, and viral vector vaccines (vaccines that contain a recombinant virus that has the genetic instructions for making antigens from a different virus)

herd immunity

resistance to the spread of an infectious disease within a population that’s based on pre-existing immunity of a high-proportion of individuals

immunotherapy

a form of medical treatment that modulates the functioning of the immune system in order to treat disease. the 2 broad categories are activation immunotherapies and suppression immunotherapies

monoclonal antibodies

antibodies produced in a lab that bind to a specific antigen. they can be used to target specific types or parts of cells for a variety of therapeutic purposes