ILOs Flashcards

1
Q

Explain anabolism, catabolism and interrelationships

A

anabolism - simple molecules are built up to produce complex molecules. requires energy through the hydrolysis of ATP. endergonic. biosytnthetic. reductive > loses electrons. diverging (same simple molecules > many varying complex molecules)
catabolism - complex molecules are broken down into simple molecules. releases energy. provides the energy for ATP production. exergonic. degradative. oxidative > gains electrons. converging (many varying complex molecules > the same by-product (simple molecules))
metabolism = anabolism + catabolism. every catabolic process requires anabolism.

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2
Q

Define oxidation and reduction

A

oxidation is the loss of electrons
reduction is the gain of electrons

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3
Q

Explain the need for stepwise oxidation of high energy molecules

A

reduction in activation energy so the reaction can proceed at 37ºC
reduces the free energy released
provides convenient control points\can be integrated with other cellular metabolism.

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4
Q

Explain the role of enzymes in reactions
a) Some conventions about the naming of enzymes

A

biological catalysts
proteins that catalyse the conversion of a substrate into a product
perform most chemical reactions in cells
enzyme name is derived from its substrate and its action

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5
Q

review the structures and functions of major carbohydrates

A

glucose - C6H12O6 - a hexose sugar containing an aldehyde group. primary energy source. oxidised to carbon dioxide and water.
monosaccharides:
triose sugar - glyceraldehyde
pentose sugar - ribose/deoxyribose
hexose sugar - mannose. galactose. fructose.
disaccharides:
sucrose - ⍺-D-glucose + fructose with an ⍺-1,2-glyosidic linkage
maltose -⍺-D-glucose + β-D-glucose with an ⍺-1,4-glyosidic linkage
cellobiose - 2x β-D-glucose with a β-1,4-glycosidic linkage
polysaccharides:
cellulose
starch and glycogen

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6
Q

describe how different catabolic pathways are interlinked

A

glycolysis > TCA cycle
beta-oxidation > TCA cycle
amino acid catabolism > TCA cycle

a) acetyl coA production > glucose - glycolysis - pyruvate - acetyl coA
b) acetyl coA oxidation > acetyl coA - TCA cycle - carbon dioxide + electrons (the final products of catabolism)

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7
Q

understand and draw a labelled diagram showing how glucose is transported into the cell

A

occurs via Na+/glucose symporters or via passive facilitated diffusion through glucose transporters.
GLUT1 > binding of glucose to the outside triggers a conformational change so that the binding site faces inwards, glucose can be released inside the cell, conformational change regenerates the binding site on the outside.

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8
Q

describe glycolysis in outline and name its central intermediate compounds

A

conversion of glucose to pyruvate
glucose + 2ADP +2Pi + 2NAD+ > 2 pyruvate + 2ATP + 2H2O + 2NADH + 2H+

glucose
glucose-6-phosphate
fructose-6-phosphate
fructose-1,6-bisphosphate
>
phosphoenol pyruvate
pyruvate

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9
Q

introduce the key regulatory mechanisms of glycolysis

A

hexokinase:
glucose + ATP > glucose-6-phosphate + ADP + H+
inhibited by glucose-6-phosphate
PHOSPHOFRUCTOKINASE
fructose-6-phosphate + ATP > fructose-1,6-bisphosphate + ADP + H+
pyruvate kinase:
phosphoenol pyruvate + ADP + H+ > pyruvate + ATP
inhibited by ATP

phosphofructokinase - the key enzyme
negatively modulated by ATP, citrate and H+
positively modulated by fructose-2,6-bisphosphate, and AMP

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10
Q

Understand the need to regenerate NAD+

A

NAD⁺ is essential for making energy (ATP).
Without NAD⁺ regeneration, glycolysis stops, and cells can’t function.
Oxygen helps regenerate NAD⁺ via the electron transport chain, but if oxygen is low, fermentation is used instead

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11
Q

Describe the different reactions pyruvate can undergo, under aerobic or anaerobic conditions

A

aerobic:
glucose > pyruvate > pyruvate oxidation - acetyl coA > TCA cycle > electron transport chain/ATP synthesis > carbon dioxide and water
anaerobic:
glucose > pyruvate > fermentation > lactate or alcohol (yeast)

lactate acid fermentation - DRAW
alcoholic fermentation - DRAW

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12
Q

Describe how pyruvate is converted to acetyl-coA

A

pyruvate enters the micochondria
the pyruvate dehydrogenase complex catalyses the oxidative decarboxylation of pyruvate to acetyl coA

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13
Q

Describe the reactions, the products, the location and the control mechanisms of the TCA cycle

A

draw TCA cycle
four oxidation reactions - NADH + H+ and FADH2
one GTP is formed
location - mitochondrial matrix

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14
Q

Reproduce a schematic diagram showing the TCA cycle and explain the fate of carbon molecules in the cycle

A

DRAW

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15
Q

Describe the links between glycolysis, the TCA cycle and oxidative phosphorylation

A

glucose > pyruvate > TCA cycle > ETC

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16
Q

Understand, draw and fully label schematic diagrams illustrating:
a) ATP synthesis resulting from the passage of high energy electrons through the mitochondrial electron transport chain
b) Activation of ATP synthase by movement of protons (H+) from the intermembrane space to the mitochondrial matrix

A

a) high energy electros are carried by NADH and FADH2 and are used to reduce oxygen to water. the energy is used to pump protons (H+) from the mitochondrial matrix to the intermembrane space. protons flow back across the membrane, following their concentration gradient. energy of proton flow is used to phosphorylate ADP to ATP.
b) electrochemical gradient of H+ across mitochondrial inner membrane where flow of protons turns the rotor of ATP synthase and causes a conformational change which results in ATP synthesis.

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17
Q

Describe electron transport by the respiratory chain and the associated transport of protons

A

four multisubunit complexes in the inner mitochondrial membrane
electrons from NADH enter at complex I and electrons from FADH2 enter at complex II
electrons are handed down from higher to lower redox potentials
electrons are transferred onto oxygen to form water
ubiquinone is hydrophobic and shuttles rapidly within the membrane
cytochrome C is soluble and is on the membrane

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18
Q

Explain how much ATP can be synthesised when a reduced cofactor is oxidised by the electron transport chain

A

26-28 ATP
6 NADH - 15 ATP
2 FADH2 - 3 ATP

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19
Q

Describe, in outline, the pathways of glycogenesis and glycogenolysis

A

glycogenesis:
synthesis of glycogen from glucose
glucose > glucose-6-phosphate > glucose-1-phosphate > UDP-glucose > [glucose]n+1 + UDP
catalysed by glycogen synthase
glycogenolysis:
breakdown of glycogen to form glucose
[glucose]n+1 + phosphate > glucose-1-phosphate + [glucose]n+1
catalysed by glycogen phosphorylase

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20
Q

Explain the role of glycogen as an energy store

A

glycogen is the main storage form of glucose in liver and muscle cell
liver glycogen - broken down between meals and released to maintain blood glucose levels for red blood cells and the brain
muscle glycogen - not available for maintanence of blood glucose levels. provides energy during bursts of physical activity.
glycogen - a polymer consisting of glucose molecules joined by ⍺-1,4-glycosidic linkages. branches are introduced by ⍺-1,6-glycosidic linkages

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21
Q

Explain how a molecule of glucose can be added to a growing glycogen molecule driving glycogen biosynthesis and the role of UDP-sugars in this process

A

glucose residues can only be added to an existing glycogen chain
UDP-glucose acts as an intermediate

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22
Q

Describe how glucose is released from glycogen

A

one glucose molecule is cleaved of the ends of glycogen at a time by glycogen phosphorylase
in the liver glucose-6-phosphate is converted to glucose and enters the blood via GKUT-2 transporter
in skeletal muscle glucose-6-phosphate enters glycolysis.

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23
Q

Describe, in outline, how glucose can be formed from non-carbohydrate precursors by gluconeogenesis, and, explain why this is particularly important in the absence of dietary carbohydrates

A

gluconeogensis - synthesis of glucose within the body from non-carbohydrate precursors
lactate - synthesised by skeletal muscle under anaerobic conditions
amino acids - derived from muscle protein by proteolysis
glycerol - derived from triglycerides by lipolysis in adipose tissue
DRAW

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24
Q

Describe, in outline, the distinction between glycogenic and ketogenic amino acids

A

glycogenic - converted into glucose via gluconeogenesis. degraded to pyruvate or TCA cycle intermediates. can be converted into phosphoenolpyruvate and then into glucose
ketogenic - converted into ketone bodies. degraded to acetyl coA or acetoacetyl coA. can give rise to ketone bodies or fatty acids.

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25
explain briefly the key steps in amino acid catabolism
after removal of the ⍺-amino group the remaining carbon skeletons are converted into major metabolic intermediates and can then be converted to glucose or oxidised in the TCA cycle 1. deamination 2. conversion to metabolic intermediates 3. urea cycle
26
Describe why fats are rich energy sources and list other requirements for them
fat is used as an energy source, for essential fatty acids, and for fat soluble vitamins.
27
Outline the steps in fat synthesis
1. lipolysis - breakdown of lipids. initial cleavage by hormone sensitive lipases which release free fatty acids and glycerol 2. fatty acid oxidation - fatty acids are converted to coA derivatives (acyl CoA) 3. beta oxidation - acyl-carnitine to acyl coA and acetyl coA which will enter the TCA cycle lipogenesis - fatty acid synthesis. carbohydrates are converted to fatty acids and triglycerides in the liver, triglycerides formed in the liver are transported to adipose tissue by VLDL for storage
28
Distinguish the metabolic processes taking place after meals from those after an overnight or prolonged fast
post prandial: after food ongoing digestion most abundant energy sources blood glucose levels rise directly due to food source post absortive: after digestion is complete 3-5 hour after meal - typically overnight blood glucose maintained by liver glycogen fasted state: a prolonged period of fasting > 12 hours glycogen depleted utilisation of gluconeogenesis
29
Glossary a) An overview of the immune system b) The anatomy of the immune system (i)Intrinsic epithelial barriers to infection (ii)Primary lymphoid tissues (iii)The lymphatic system (iv)Secondary lymphoid tissues c) Cellular components of the immune system (i)Innate immune system (ii)Adaptive immune system d) Molecules of the immune system (i)Antigens and antibodies (ii)Complement system proteins (iii)Cytokines e) Overview of immune responses to pathogens
1. The immune system defends the body against harmful invaders like bacteria, viruses, and other pathogens. It has two main components: innate immunity (the body's first line of defense) and adaptive immunity (which provides a more specific and lasting defense). 2. a. Intrinsic epithelial barriers to infection: These include physical and chemical barriers such as the skin, mucous membranes, and secretions (like saliva, tears, and stomach acid) that help prevent pathogens from entering the body. b. Primary lymphoid tissues: These are where immune cells are created and mature. They include the bone marrow (where blood cells are produced) and the thymus (where T-cells mature). c. The lymphatic system: A network of vessels and organs that transport lymph (a fluid containing white blood cells) and helps in the removal of waste and pathogens from the body. It includes lymph nodes, spleen, and tonsils. d. Secondary lymphoid tissues: These are where immune responses are initiated and include structures like lymph nodes, spleen, tonsils, and mucosal-associated lymphoid tissues (MALT). They filter lymph and trap pathogens. 3. a. Innate immune system: The first line of defense against infections. It includes physical barriers (e.g., skin), immune cells (e.g., macrophages, neutrophils), and molecules (e.g., cytokines) that act immediately after infection. b. Adaptive immune system: Provides a more specific and long-lasting defense. It involves T-cells (which help control immune responses) and B-cells (which produce antibodies to neutralize pathogens). 4. a. Antigens and antibodies: Antigens are molecules found on pathogens (or abnormal cells) that trigger an immune response. Antibodies are proteins produced by B-cells that recognize and bind to specific antigens to neutralize or mark them for destruction. b. Complement system proteins: A group of proteins that work with antibodies to help destroy pathogens by promoting inflammation, enhancing phagocytosis, and directly attacking pathogens. c. Cytokines: Small proteins that are crucial in cell signaling during immune responses. They help regulate immune cell functions like activation, growth, and differentiation. 5. a.Recognition of the Pathogen: The immune system identifies pathogens (like bacteria, viruses, fungi, and parasites) using pattern recognition receptors (PRRs) that detect common molecular structures on pathogens, known as pathogen-associated molecular patterns (PAMPs). b.Innate Immune Response: i. First line of defense: This includes physical barriers (like skin and mucous membranes) and cellular components (like macrophages, neutrophils, and dendritic cells). ii. Inflammation: When a pathogen is detected, immune cells release cytokines to recruit other immune cells to the site of infection, causing redness, swelling, heat, and pain. iii. Phagocytosis: Cells like macrophages and neutrophils engulf and digest the pathogen. iv. Complement system: Activated by antibodies or pathogen surfaces to promote inflammation, phagocytosis, and direct destruction of the pathogen. c. Adaptive Immune Response: i. T-cell activation: Dendritic cells present antigens to T-cells in lymph nodes, activating them. Helper T-cells (TH cells) coordinate the immune response, while cytotoxic T-cells (CTLs) destroy infected cells. ii. B-cell activation: When B-cells encounter their specific antigen, they differentiate into plasma cells that produce antibodies. These antibodies bind to pathogens, neutralizing them and marking them for destruction by other immune cells. iii. Memory: After the pathogen is cleared, memory T-cells and memory B-cells are formed. These cells “remember” the pathogen and can mount a faster and stronger response if the pathogen is encountered again.
30
Appreciate the importance of the immune system and that abnormal immune responses can lead to disease (allergy, autoimmunity)or transplant rejection
the immune system protects from pathogens and abnormal cells is a complex network of specialised cells, tissues and soluble factors that cooperate to kill and eliminate microorgansims and cancerous cells - by distinguishing self molecules from non-self molecules, or by identifying danger signals from acute inflammation immune overreaction - reaction to self (autoimmunity), reaction to innocuous substances (allergies), rejection of donor tissues (transplantation) immune underreaction - recurrent infections, cancer. the immune system protects against pathogens and abnormal cells. Malfunctioning immune responses can cause allergies, autoimmune diseases, and transplant rejection.
31
Understand the role of constitutive barriers in defending the body against invading pathogens
These are the body’s first line of defense (e.g., skin, mucous membranes, stomach acid) against pathogens.
32
Describe the key differences between the innate and adaptive immune systems
Innate Immunity: Quick, general defense; non-specific; includes barriers, macrophages, mast cells, etc. Adaptive Immunity: Slower, specific response; includes T-cells and B-cells that recognize specific antigens and form memory.
33
Understand how components of the innate immune system become activated by invading microorganisms
Pathogen-associated molecular patterns (PAMPs) on pathogens are recognized by pattern recognition receptors (PRRs) like TLRs (Toll-like receptors)
34
Describe how tissue-resident and circulating innate immune cells (macrophages, mast cells, natural killer cells, neutrophils) respond to invading pathogens and/or tissue damage; a) How do they recognise invading pathogens b) How do they kill extracellular pathogens or virally-infected host cells
Macrophages, mast cells, NK cells, neutrophils: a. Recognize pathogens via PRRs or antibodies. b. Kill pathogens through phagocytosis or cytotoxicity (e.g., NK cells killing infected cells).
35
Describe how systemic effects of acute inflammation stimulates other innate immune responses to protect the body against invading pathogens; a) The acute phase response b) The complement system c) Dendritic cell activation
Triggers systemic immune responses to fight pathogens. a. Acute phase response: Activation of proteins like CRP to mark pathogens. b. Complement system: Proteins that help destroy pathogens. c. Dendritic cell activation: Helps bridge innate and adaptive immunity.
36
Understand how dendritic cells function as a ‘bridge’ between the innate and adaptive immune systems
Dendritic cells process and present antigens to T-cells, bridging innate and adaptive immunity.
37
Describe the differences between innate and adaptive immunity, emphasising specificity, memory and diversity
Innate: Non-specific, fast, no memory. Adaptive: Specific, slower, forms memory, and has a diverse range of responses.
38
Explain how antigen receptors on T cells and B cells recognise antigens with specificity
T-cells recognize MHC-presented antigens. B-cells recognize free-floating antigens (or those attached to pathogens).
39
Outline the processes of clonal selection and clonal expansion, including the role of the cell cycle in lymphocyte proliferation
Upon recognizing their specific antigen, lymphocytes (T/B-cells) proliferate and differentiate into effector cells.
40
Discuss the interactions between T-cells and the role of antigen presentation by MHC I and MHC II molecules
MHC I presents intracellular antigens to CD8+ T-cells. MHC II presents extracellular antigens to CD4+ T-cells.
41
How do T cells recognise antigens
T-cells use their T-cell receptors (TCRs) to recognise antigens presented by MHC molecules on other cells.
42
What happens when antigens are recognised by T cells
T-cells become activated and differentiate into effector cells, cytotoxic T-cells or helper T-cells
43
What effector cells do naïve T-cells become
CD4+ T-cells become helper T-cells, aiding other immune cells. CD8+ T-cells become cytotoxic T-cells, killing infected or cancerous cells.
44
Explain the mechanisms behind B cell activation in lymphoid tissues
In lymphoid tissues, B-cells recognise antigens directly and, with the help of helper T-cells, become activated and proliferate.
45
Understand the importance of germinal centres
These are the areas in lymphoid tissues where B-cells undergo mutation and selection, leading to high-affinity antibodies.
46
Outline class switching and affinity maturation
Class switching: B-cells can change the type of antibody they produce (e.g., from IgM to IgG, IgA, or IgE) without changing their specificity for the antigen. Affinity maturation: B-cells undergo mutations to increase the affinity of their antibodies for the antigen, improving their effectiveness.
47
Differentiate the roles of plasma cells and memory B cells
Plasma cells: Secrete large quantities of antibodies to fight current infections. Memory B cells: Remain in the body for years, ready to respond faster if the same antigen is encountered again.
48
How do B cells recognise antigens
B-cells have receptors (BCRs) that bind directly to antigens, typically from pathogens, leading to activation.
49
How do T cells help B cells produce antibodies
Helper T-cells (specifically TH2 cells) activate B-cells by providing co-stimulatory signals and cytokines, promoting their differentiation into plasma cells.
50
What are the structure and functions of antibodies
Structure: Antibodies are Y-shaped proteins with a variable region (that binds to antigens) and a constant region (that interacts with immune cells). Functions: Antibodies neutralize pathogens, opsonise them for phagocytosis, and activate the complement system.
51
How are highly specific antibodies produced against antigens
B-cells undergo somatic hypermutation in germinal centers, where they generate a diverse range of antibodies and select the ones with the highest affinity for the antigen
52
Understand antigens and co-stimulatory molecules play a key role in lymphocyte activation
Antigens bind to receptors on lymphocytes, initiating activation. Co-stimulatory molecules (like CD80/86 on antigen-presenting cells) are required for full lymphocyte activation, ensuring an appropriate immune response.
53
Understand lymphocyte activation leads to increased expression of key transcriptional targets to promote; a) Cell cycle entry and clonal expansion (proliferation) b) Metabolic adaptation c) Differentiation into effector cells
a. Cell cycle entry & clonal expansion: Lymphocytes proliferate to generate a large number of identical cells for a stronger immune response. b. Metabolic adaptation: Lymphocytes adjust their metabolism to support increased activity and energy needs. c. Differentiation into effector cells: Lymphocytes differentiate into specific effector cells to combat the pathogen (e.g., cytotoxic T-cells, plasma cells).
54
Understand functions of terminally differentiated, effector lymphocytes; a) Cytotoxic T cells (CTLs) b) T helper 1 cells (TH1 cells) c) T helper 2 cells (TH2 cells) d) T follicular helper cells (TFH cells) e) Plasma cells (and antibodies)
a) Cytotoxic T-cells (CTLs): Kill infected cells by inducing apoptosis. b) T helper 1 cells (TH1): Activate macrophages and promote inflammation, helping to fight intracellular pathogens. c) T helper 2 cells (TH2): Help B-cells produce antibodies and assist in the defense against parasites and allergens. d) T follicular helper cells (TFH): Provide help to B-cells in germinal centers, promoting antibody production. e) Plasma cells: Secrete large amounts of antibodies to neutralize pathogens.
55
Human relationship to agriculture/plants a) What are the four major crops b) How much land is devoted to agriculture
a) maize (corn), rice, wheat, potatoes b) 45% of habitable land is used for agriculture
56
How did we get here? (Plant sciences) a) What is the process of crop domestication b) What genes and traits were modified in crops c) Case study - rice and maize
a) wild cereal is cultivated and domesticated into landraces where selective breeding occurs to form modern cereal. b) domestication of cereals selected for developmental traits that increase growth yield; loss of shattering, loss of grain dispersal aids, increase in grain size, loss of sensitivity to environmental cues for germination and flowering, synchronus tillering and ripening, compact growth habitat, enhanced cullinary chemistry. c) the rice gene qSH1 controls abscission zone formation at the base of rice flower. single nucleotide polymorphism (SNP) in 5' regulatory region of a single transcription factor was responsible for nonshattering rice two maize genes that both encode a transcription factor > teostine glume architecture promotes development of tough case around kernel, and teostine branched 1 suppresses branching to promote single stalk.
57
the green revolution a) What is the population bomb b) Why were dwarf crop varieties important c) What plant hormone signalling was involved in the green revolution
a) ?? b) green revolution and intense farming practices pushed yields higher c) green revolution varieties had defective gibberellin hormone biosynthesis or perceptrion
58
Submergence tolerant rice a) What are the challenges in lowland rice b) What type of traits are desirable in lowland environments c) What genes are involved in submergence tolerant rice d) What are the signalling pathways and factors involved in submergence tolerant rice e) How did MAS accelerate breeding of elite Sub1a rice
a) flooding b) flood tolerance/submergence tolerance c) sub1a transgene d) ethylene signalling pathway to inhibit gibberellin response e) involved selecting for DNA markers as it is faster than waiting for phenotypic expression
59
Describe plant anatomical structures that play an important role in signalling
cell wall - provides structure to the pland cell and bonds with other cell walls to form the structure of the plant plasmodesmata - traverse the cell walls of plant cells, enabling transport and communication between plant cells, regulated by callose deposition in the cell wall. xylem - transports water and mineral salts from the roots up to other parts of the plant phloem - transports sucrose and amino acids between the leaves and other parts of the plant
60
Understand that plants can respond to their environment through various types of signals
symplastic transport - uses plasmodesmata that interconnect the cytoplasms of neighbouring cells apoplastic transport - involves passive diffusion of molecules in the extracellular space and the cell wall transcellular transport - combines apoplastic transport with a secretion, and, endocytosis-based or channel and carrier-based transport pathway to cross plasma membrane. the ROS wave glutamate
61
Describe the role that different classes of receptors play in pathogen perception an downstream signalling a) PRR’s vs NLR’s
PRRs: PRRs are found on the cell surface and recognize PAMPs (Pathogen-Associated Molecular Patterns)—molecules that are conserved across many microbes but absent in the host. PRRs trigger PAMP-Triggered Immunity (PTI), which strengthens the plant’s defenses and prevents infection 1. PRRs recognize PAMPs → Activate receptor-like kinases (RLKs). 2. ROS (Reactive Oxygen Species) production → Helps kill microbes. 3. MAPK (Mitogen-Activated Protein Kinase) activation → Turns on defense genes. 4. Callose deposition → Strengthens the cell wall to block pathogen entry. 5. Defense-related gene expression → Produces antimicrobial compounds. NLRs: NLRs are intracellular receptors that recognize pathogen-secreted effector proteins. These effectors help pathogens suppress PRR-mediated immunity, but NLRs detect their presence and trigger a stronger immune response called Effector-Triggered Immunity (ETI). ETI often leads to programmed cell death (Hypersensitive Response, HR), which stops pathogen spread 1. NLRs recognize effector proteins inside the host cell. 2. Triggers a hypersensitive response (HR) → Infected cells undergo programmed cell death to stop pathogen spread. 3. Activates salicylic acid (SA)-dependent signaling, reinforcing systemic immunity.
62
Explain how pathogen perception leads to enhanced defences
the activation of enhanced plant defenses, which include cell wall strengthening, antimicrobial compound production, and programmed cell death to prevent pathogen spread. Plants feature a multilayer defence system. * Recognition of conserved pathogen molecules (MAMPs/PAMPs) by specific receptors (PRRs) triggers signalling cascades and defences. * Defence signalling involved production of ROS, ion fluxes, MAPK signalling cascades and leads to changes in gene expression. * Recognition of MAMPs evolved independently in plants and mammals. * Pathogens deliver molecules, called effectors, inside their host to interfere with plant defences. * Plants can recognize these effectors using another class of receptors called NLRs. * Similar immune receptors, with a unique conserved structure, evolved independently in mammals.
63
Explain the key differences, as well as, similarities between the plant and animal innate immune system
Both plants and animals have innate immunity with similar defense mechanisms such as PRRs, PAMP detection, ROS production, and cell death. Plants rely entirely on their innate immune system, while animals have both innate and adaptive immunity. Plants use structural barriers and chemical defenses, whereas animals use mobile immune cells and systemic responses.
64
To review common routes of infection and prevention mechanisms
physical barriers to infection skin - keratin, sebum (oil) langerhans cells can phagocytose microbes and form part of the skin-associated lymphoid tissue mucous membranes - trap and destroy pathogens. mucous layers slough off, removing pathogens. cilia remove microbes from the lungs. gut-associated lymphoid tissue - tonsils, adenoids and peyers' patch, specialised M cells. chemical barriers to infection: defensins - cationic peptides that destroy the cytoplasmic membrane of microbes.
65
To overview koch’s postulates and the implications
1. the microorganism must be found in abundance in all organsims suffering from the disease but should not be found in healthy animals 2. the microorganism must be isolated from a diseased organism and grown in pure culture 3. the cultured microorganism should cause disease when introduced into a healthy organism 4. the microorganism must be re-isolated from the innoculated, diseased, experimental host and identified as being identical to the original microorganism.
66
Introduce how the bacterium helicobacter causes infections
ingestion - flagella propel pathogen to mucosa urease production - converts urea to carbon dioxide and ammonia to reduce acidity in the local area enzyme production - to soften the mucous lining allowing access to epithelial layer the lower level of acidity allows growth and division of bacterium, causing inflammation and damage to the stomach lining.
67
Understand common STIs and how selected organisms do not conform to koch’s postulates
chlamydia syphilis pseudomembranous colitis clostridioides difficile
68
Describe the exceptions to koch’s postulates and how the ‘framework’ has been refined
microorganisms that are unable to be cultured on artificial media when two or more organisms work insynergy to cause a disease symptoms or diseases that can be caused by several microbes ethical exceptions (i.e. cannot perform the experiments) highly contagious, virulent, or dangerous strains infection can be asymptomatic
69
Understand how microbes are classified
molecular methods utilising SSU rRNA three distinct domains of life - archaea, bacteria, eukarya well conserved genes - 16S rRNA, 23S rRNA, ITS region, gyrB taxonomy > domain - kingdom - phylum - class - order - family - genus - species
70
Define key principles of the microbiome
the combined genetic material of the microorganisms in a particular environment the microorganisms in a particular environment.
71
Understand how the microbiome is investigated
amplicon sequencing of the 16S rRNA gene for bacteria or the ITS for fungi microbial potential < metabolic potential < microbial function cells < DNA < RNA < protein < metabolite alpha diversity - a measure of how diverse a sample is based on, how many species there are, and how abundant each species is within a sampled environment beta diversity - a measure of how different- or similar - two samples are to each other
72
Understand the concept that viruses are not independent lifeforms but are obligate intracellular parasites
viruses are not alive, they are obligate intracellular parasites that infect all forms of life
73
Know the range of genome types, capsid organisation and size of viruses
simple forms of virions - naked icosahedral capsid, enveloped icosahedral, naked helical nucleocapsid, enveloped helical nucleocapsid 1. type of nucleic acid - RNA or DNA 2. strandedness - single or double stranded 3. linear or circular 4. sense - positive or negative 5. number of segments 6. nucleotide sequence DNA molecules - linear single stranded, circular single stranded, linear duplex, duplex with closed ends, closed circular duplexes. RNA molecules - linear,single stranded infectious "positive" strand, linear,single stranded non-infectious "negative" strand, segmented positive strands, segmented negative strands, double stranded segment, diploid single strands
74
Understand what is meant by ‘plus’ and ‘negative’ strand RNAs, and that, once inside a cell, the genomes of plus strand RNA viruses are infectious, while the genomes of negative strand RNA viruses are not infectious
RNA molecules - linear,single stranded infectious "positive" strand, linear,single stranded non-infectious "negative" strand, segmented positive strands, segmented negative strands, double stranded segment, diploid single strands
75
Discuss viral latency and the sites where latent viruses are held in relation to herpes simplex virus
mild pharyngitis fever is the primary infection, following this the virus transit up the peripheral nerve where it is latent following activation and subsequent recurrence a cold sore occurs.
76
Understand how the same varicella zoster virus can cause clinically distinct diseases I.e. chickenpox and shingles
primary infection is chickenpox following recurrence, shingles occurs
77
Understand how to protect against virus disease using vaccination and anti-viral therapy
a vaccine is a biological preparation that improves immunity to a particular disease. a vaccine typically contains a small amount of an agent that resembles a microorganism. the agent stimulates the bodys immune system to recognise the agent as foreign, destroy it, and 'remember' it, so that the immune system can more easily recognise and destroy any of these microorganisms that it later encounters neuraminidase inhibitor - inhibits virion release and therefore halts viral replication oseltamivir - slows the spread of influenza virus between cells by stopping the virus from chemically cutting ties with its host cell zanamivir - binds to the active site of neuraminidase rendering the influenza virus unable to escape its host cell and infect others
78
Understand how influenza virus is transmitted
respiratory or saliva spread airborne droplets direct contact surface contamination
79
Know the structure of the influenza virion
The influenza virion consists of an envelope containing glycoproteins (hemagglutinin and neuraminidase), a matrix protein, a nucleocapsid with RNA segments and associated proteins, and a polymerase complex
80
Know the nature of the membrane surrounding the virion and viral proteins integrated into the membrane
The influenza virion is an enveloped virus, meaning it has a lipid bilayer membrane that surrounds the viral particle. This membrane is host-derived because the virus takes a portion of the host cell’s membrane during the process of budding out of the infected cell. The lipid bilayer serves as a protective barrier, helping the virus evade the host’s immune system and facilitating the fusion of the virus with host cell membranes during infection. Hemagglutinin (HA): This is a spike-like protein that is responsible for the virus's ability to bind to and enter host cells. HA recognizes and binds to sialic acid receptors on the surface of host cells, facilitating viral entry. Neuraminidase (NA): This is another spike-like protein involved in the release of new viral particles. NA cleaves sialic acid residues from glycoproteins on the host cell surface and from viral particles themselves, preventing clumping and allowing the virus to spread to other cells.
81
Know which viral proteins are the targets for neutralising antibodies
hemmagglutinin neuraminidase
82
Know that influenza has a segmented, negative sense, RNA genome
influenza has a segmented, negative sense, RNA genome
83
Understand how gradual changes are responsible for genetic drift and how this leads to seasonal outbreaks of ‘flu’
antigenic drift - existing antigens are subtly altered. causes slight flu mutations year on year, from which humans have partial, but not complete immunity. antigenic shift - two or more strains combine.
84
Understand the dramatic reassortment of viral genome segments, often from other species of host, that lead to new pandemic viruses
Swine serve as "mixing vessels" for the genes of avian, porcine and human forms of the influenza virus. In the host pig, the avian and mammalian viruses can share (reassort) their genes and so create new strains of flu. Swine have probably played an important role in the history of human influenza epidemics.
85
Name some of the virus infections that have emerged, or re-emerged, in the recent past
zika ebola H1N1 influenza COVID 19
86
Understand the epidemiology of coronavirus infection; a) How it is transmitted b) What are the time scales involved c) How SARS-Cov-2 emerged
a) after a sneeze, large droplets of saliva and mucous shoot out of the mouth, but fall relatively quickly. a turbulent cloud carries smaller droplets and allows them to drift for up to 8 meters. b) incubation period - 2>14 days. infectious period - 1>2 days before symptoms appear and remain contagious for about 10 days c) emerged from a zoonotic spillover
87
Discuss the development of effective vaccines that protects against coronavirus infection
oxford uni - astrazeneca = viral vector vaccine (genetically modified virus), 2 doses, stored at fridge temp pfizer - bioNtech = RNA vaccine (part of virus genetic code), 2 doses, stroed at -70ºC moderna - RNA vaccine, 2 doses, stored at -20ºC
88
Understand how tests for SARS-Cov-2 detect either viral nucleic acid or antibodies against viral proteins, what are their advantages and disadvantages
PCR: detect viral RNA in a sample high sensitivity and reliable time-consuming and costly lateral flow test: detect antigens quick results and easy to use lower sensitivity and specificity RT-LAMP: detects viral RNA high sensitivity and rapid results limited availability
89
Understand how coronavirus gets into particular cells and understand mechanism of entry
human angiotensin-converting enzyme 2 (ACE2) is the receptor for coronavirus Spike protein binds to ACE2 receptor on host cell. Virus enters the host cell via fusion or endocytosis. The viral RNA is released into the host cell, hijacking its machinery to produce more virus.
90
Understand the nature of the coronavirus particle and its genomic nucleic acid
Coronaviruses form enveloped and spherical particles of 100-160nm in diameter. Contain a positive sense, single stranded RNA genome of 27-32 kb The 5’ terminal 2/3 of the genome encodes a polyprotein, pp1ab which is further cleaved into 16 non-structural proteins involved in genome replication and transcription The 3’ terminal 1/3 of the genome encodes structural proteins including envelope glycoprotein spike (S), envelope (E), membrane (M) and nucleocapsid (N) Spike protein binds to receptor on cell surface