t2 cells Flashcards

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1
Q

what is the cell wall of a plant made of & it’s function

A

cellulose - provides structure and support to the cell

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2
Q

what are plasmodesmata

A

pores that connect two neighbouring plant cells and enable exchange through the cytoplasm

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3
Q

what is the cell surface membrane formed by

A

phospholipid bilayer - partially permeable to allow exchange (of lipid soluble) substances directly through it

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4
Q

what is a histone

A

proteins that DNA wraps around to form compacted coil shape

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5
Q

features of the nucleus and their functions

A
  • double membrane called nuclear envelope that has many nuclear pores that allow mRNA and ribosomes to travel out of the nucleus, as well as allowing enzymes and molecules in
  • chromatin - material (DNA and histones) which make up chromosomes
  • nucleolus - makes ribosomes
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6
Q

structure and function of mitochondria

A
  • site of aerobic respiration
  • has double membrane, with inner membrane folded to form cristae
  • has liquid called matrix which contains enzymes needed for aerobic respiration, producing ATP and also contains small pieces of DNA and ribosomes
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7
Q

structure and function of chloroplast

A
  • site of photosynthesis in plant cells.
  • have double membrane
  • grana - thylakoid membranes that stack
  • lamellae - think thylakoid membranes that join grana together
  • contain small pieces of DNA and ribosomes to synthesise proteins needed for chloroplast replication and photosynthesis
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8
Q

function of ribosomes + how they’re made

A
  • site of translation in protein synthesis
  • found freely in cytoplasm or as part of the RER
  • formed in the nucleolus and made of rRNA and proteins.
  • can be 80S (in eukaryotic cells) or smaller 70S (in prokaryotic cells, mitochondria and chloroplasts)
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9
Q

structure and function of rough endoplasmic reticulum (RER)

A
  • folds and processes proteins made at the ribosomes located on its surface and sends them to the golgi apparatus.
  • made of flattened, membrane-bound sacs (cisternae) stacked together around the nucleus
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10
Q

structure and function of smooth endoplasmic reticulum (SER)

A
  • synthesises and processes lipids, carbs and steroids and sends them to the golgi apparatus
  • made of flattened, membrane-bound sacs.
  • NO ribosomes on surface
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11
Q

structure and function of golgi apparatus

A
  • further processes and packages lipids and proteins from the ER into vesicles or lysosomes
  • flattened stack of fluid-filled, membrane-bound sacs (cisternae)
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12
Q

structure and function of vacuole

A
  • maintains pressure in plant cells by pushing cytoplasm against cell wall to keep cell turgid and prevent plants from wilting
  • contains cell sap
  • has selectively permeable membrane called tonoplast
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13
Q

structure and function of lysosomes

A
  • digest invading cells and break down worn out cells/organelles (autolysis)
  • contain lysozymes (digestive enzymes)
  • small, spherical sacs formed by the golgi apparatus
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14
Q

structure and function of the centriole

A
  • organises spindle fibres during cell division
  • hollow fibres made of microtubules
  • 2 centrioles at right angles form a centrosome
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15
Q

what is the cell wall made of in prokaryotic cells

A

murein/peptidoglycan (protein and polysaccharide combined)

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16
Q

structure and function of mesosomes

A
  • in prokaryotic cells
  • invagination of the cell membrane
  • permeable boundary that allows for entry and exit of nutrients and waste and may play a role in DNA replication
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17
Q

structure and function of pilli

A
  • in prokaryotic cells
  • thin, protein tubes on surface of bacteria
  • allow bacteria to adhere to surfaces
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18
Q

structure and function of capsid

A
  • in viral cells
  • protein coat
  • protects the genetic material
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19
Q

function of attachment proteins on viral cells

A
  • identify and attach to host cells for viruses to replicate inside of
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20
Q

what is the viral genome

A
  • nucleic acid core made of DNA or RNA
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21
Q

what is the lipid envelope on viral cells

A
  • viruses sometimes take a piece of the cell membrane with them as they leave the host cell, causing them to have a lipid envelope around their capsid
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22
Q

why don’t antibiotics work on viruses

A
  • antibiotics target the bacterial enzymes and ribosomes and interfere with the bacteria’s metabolic reactions
  • viruses don’t have their own enzymes or ribosomes
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23
Q

definition of resolution

A

ability to distinguish between two points on an object - minimum distance that this can be done

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24
Q

definition of magnification

A

how much larger the image is than the specimen

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25
Q

features of optical (light) microscopes

A
  • uses light waves that have a relatively long wavelength, meaning their resolution is lower (max: 0.2 micrometers)
  • lower mag (max: x1500)
  • can view living organisms
  • can view in colour
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26
Q

features of electron microscopes

A
  • uses electron beams that have a relatively short wavelength, meaning their resolution is much higher (max: 0.1 nanometres)
  • electron beams directed using electromagnets due to their negative charge
  • higher mag (max: x1.5 million)
  • can’t view living organisms as required near vacuum so electrons aren’t deflected or absorbed by air particles
  • specimen must be extremely thin and go through a complex staining process
  • artefacts may appear on photomicrograph eg dust, cotton fibres
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27
Q

features of transmission electron microscopes (TEM)

A
  • beams of electrons pass through specimen. denser parts of specimen absorb electrons and image appears darker on the photomicrograph. less dense parts let electrons pass and appear lighter on photomicrograph.
  • higher res (max: 0.1nm)
  • sample must be extremely thin
  • 2D images only
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28
Q

features of scanning electron microscope (SEM)

A
  • scans beams of electrons across the surface of specimen back and forth in a regular pattern. electrons are then collected in a cathode ray tube and used to produce photomicrograph
  • can be used on thicker specimens as electrons can be scattered by specimen
  • 3D images
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29
Q

stages of cell fractionation

A
  1. homogenisation - grind cell using blender/pestle and mortar to break open cell and release organelles. results in a fluid called the homogenate
  2. add cold, isotonic, buffered solution
  3. filtration - filter solution through gauze to remove any whole cells or debris and collect in test tube
  4. ultracentrifugation- place test tube of homogenate into centrifuge and spin on a low speed. the densest organelle (nuclei) will collect at the bottom of the test tube. pour out remaining supernatant (fluid remaining) into a new test tube.
  5. repeat step 4 using a higher speed between each separation until the least dense organelles have been separated (ribosomes)
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30
Q

order of pellet formation in cell fractionation

A

nucleus (densest)
chloroplast
mitochondria
lysosomes
endoplasmic reticulum
ribosome (least dense)

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31
Q

stages of interphase (brief)

A
  1. G1 - signal
    2.S - DNA rep
    3.G2 - check
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32
Q

what happens in G1

A

-signal received by cell to replicate
-all cell content (except chromosomes) replicate.
-makes RNA, enzymes and proteins needed for growth

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33
Q

what happens in S phase of interphase

A

-synthesis of DNA (chromosome replication)
-makes 2 identical strands of DNA called chromatids that are joined at centromere

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34
Q

what happens in G2 of interphase

A

-cell continues to grow
-synthesised DNA is checked for mutations and any copying errors and makes any repairs

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35
Q

stages of mitosis (brief)

A

1.Prophase
2.Metaphase
3.Anaphase
4.Telophase
5.Cytokinesis

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36
Q

what happens in prophase (mitosis)

A

-chromosomes condense, become visible
-spindle fibres move towards opposite poles of cell

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37
Q

what happens in metaphase (mitosis)

A

-chromosomes line up at equator of cell
-spindle fibres attach to centromeres

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38
Q

what happens in anaphase (mitosis)

A

-spindle fibres shorten
-sister chromatids pulled to opposite poles of cell as centromere divides

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39
Q

what happens in telophase (mitosis)

A

-chromosomes at opposite poles
-uncoil, become longer, not visible
-spindle fibres break down

40
Q

what happens during cytokinesis (mitosis)

A

-cytoplasm divides and 2 genetically identical daughter cells formed
-one newly formed nucleus in each

41
Q

importance of mitosis

A

-replacement of cells and repair of tissues
-asexual reproduction
-growth of multicellular organisms

42
Q

root tip squash practical

A
  1. place root tip in warmed HCl for 5 mins to hydrolyse middle lamella
    2.rinse in cold water and pat dry
    3.cut 2mm off tip and place on microscope slide
    4.add stain
    5.gently squash root tip to produce very thin layer. push straight down to prevent cells rolling together and chromosomes being damaged
    6.view under microscope and cells undergoing mitosis can be drawn
43
Q

what genes control rate of mitosis (brief)

A

1.proto-oncogenes
2. tumour suppressor genes

44
Q

proto-oncogenes (cancer)

A

-normally help cell grow
-if damaged/mutated/too many of them, gene is permanently switched on and cell grows out of control as cell cycle is sped up

45
Q

tumour suppressor genes (cancer)

A

-normally slow down cell division as they code for proteins that regulate cell cycle
-mutations = uncontrollable cell division

46
Q

treatments for cancer (what do they interrupt)

A

-interrupt interphase - prevent synthesis of enzymes needed for DNA rep or produce damaged DNA
-interrupt metaphase - spindle fibres dont form correctly
-interrupt anaphase - prevent spindle fibres from shortening

47
Q

differences between benign and malignant tumours

A

benign -
- have capsule (contained)
-low mitotic index so grow slowly
-cant metastasise
-differentiated

malignant -
-not encapsulated
-high mitotic index so grow quickly
-can metastasize
-undifferentiated

48
Q

stages of binary fission

A

1.circular DNA replicates and both copies attach to cell membrane. plasmids also replicates
2. cell membrane grows between two DNA mols and pinches inwards, dividing into 2
3.2 daughter cells are produced, each w a copy of DNA and variable no of plasmids

49
Q

replication of viruses

A

1.attachment proteins attach to receptors on host cell
2.viral nucleic acid injected into host
3.nucleic acid replicated inside host
4.reverse transcriptase makes DNA from RNA
5.host cell produces viral proteins, enzyme and capsid and assembles them

50
Q

how do prokaryotic cells divide (brief)

A

binary fission

51
Q

why is the cell surface membrane described as fluid mosaic model

A

fluid: phospholipids and proteins can move around/are flexible
mosaic: scattered pattern produced by the proteins within phospholipid bilayer

52
Q

role of phospholipids in CS membrane

A

-make up bilayer w hydrophobic tails (fatty acid chains) facing inwards and hydrophilic heads pointing outwards
-allow LIPID-soluble substances to diffuse through
-act as barrier to non-lipid soluble/water-soluble substances
-ensures sugars, amino acids, proteins cant leak out of cell

53
Q

role of cholesterol in CS membrane

A

-oriented w hydrophobic head outwards and hydrophilic heads in and fit in between phospholipids
-regulates fluidity by stabilising phospholipids by causing them to pack closely together in high temps and prevent them from being too close in cool temps
-prevent water loss as they’re very hydrophobic

54
Q

role of glycolipids and glycoproteins in CS membranes

A

-acts as receptors as they exist extrinsically which allows them to bind w certain substances eg. hormones, neurotransmitters, identify blood groups

55
Q

role of proteins in CS membrane

A

-channel proteins - water filled tubes that allow WATER-soluble substances to diffuse by facilitated diffusion

-carrier proteins - bind to ion/mol and change shape to move substance across membrane by facilitated diffusion. used when substances need to move against conc grad using active transport or cotransport

56
Q

role of aquaporins in CS membranes

A

-type of channel protein that transport water by facilitated diffusion
-have hydrophilic pores that allow water to move through them

57
Q

where is there a high number of aquaporins

A

kidneys

58
Q

what is simple diffusion

A

-movement of mols from a higher conc to a lower conc
-passive

59
Q

what is facilitated diffusion and why is it needed

A

-movement of mols from higher conc to lower conc using a carrier/channel protein
-happens when mol cannot diffuse through membrane due to polarity, size or charge
-passive

60
Q

what is active transport

A

-movement of mols from lower conc to higher conc using ATP from respiration
-uses carrier proteins
-ATP and substance bind to carrier protein and ATP hydrolysed to ADP and Pi, carrier protein changes shape and allows substance through. Pi then recombines w ADP to form ATP in respiration

61
Q

what is active transport used in

A

-absorption of maximum products of digestion
-reabsorption of useful mols/ions after filtration into kidney tubules
-transferring sugar from photosynthesising cells of leaves into phloem for transport
-transferring inorganic ions from soil into root hair cells

62
Q

3 factors affecting rate of active transport

A
  1. speed of individual carrier proteins
  2. no of carrier proteins
  3. rate of respiration in cell (ATP availability)
63
Q

what is co-transport

A

-coupled movement of substances across cell membrane via carrier protein
-combination of active transport and facilitated diffusion

64
Q

how are glucose and amino acids transported across cell membranes in intestine

A

-cotransport with sodium IONS
-transported into intestinal epithelial cells by facilitated diffusion
-the conc grad that allows for facilitated diffusion is maintained by active transport of sodium OUT of intestinal cell by sodium-potassium pump that transport sodium into capillaries.

65
Q

what is osmosis

A

-movement of water across a selectively permeable membrane from a region of higher WP to region of lower WP

66
Q

what is a hypotonic cell

A

-WP inside cell is LOWER than outside
-so net movement INTO cell
-cell becomes turgid and swells - may burst (lyse)

67
Q

what is an isotonic cell

A

-WP is equal on both sides of membrane
-no net movement of water

68
Q

what is a hypertonic cell

A

-WP inside cell is HIGHER than outside
-net movement OUT of cell
-cell becomes flaccid and shrinks

69
Q

what happens when plant cells become hypertonic

A

-plasmolysis - membrane shrinks away from cell wall

70
Q

what is ficks law

A

SA x conc grad/thickness of membrane

71
Q

what are phagocytes

A

-WBCs
-continuously produced in bone marrow and distributed around body
-non-specific so target any non-self cells and remove dead cells

72
Q

process of phagocytosis

A

1.chemo-attractants on pathogen attract phagocyte
2.phagocyte engulfs pathogen
3.phagosome vesicle forms around pathogen
4.lysosome fuses w phagosome and releases lysozymes (hydrolytic enzymes) which digests pathogen
-phagocytes present pathogen antigens on cell surface to activate T-helper cells

73
Q

structure of antibodies

A

-globular glycoproteins
-quaternary structure w two ‘heavy’ (long) polypeptide chains bonded to two ‘light’ (short) chains by disulphide bonds
-have constant regions and variable regions (different for every antibody due to primary amino acid sequence)
-antigen binding site at end of each Y shaped area (variable region - specific to one antigen)

74
Q

what type of cells involved in cell-mediated immune response + where do they mature(brief)

A

T-cells/lymphocytes
-leave bone marrow to mature in the thymus

75
Q

how are T-cells activated

A

-respond to antigens presented on antigen-presenting cells (APCs) - not antigens detached from cells
-bind to specific antigen on APC (cell that has been invaded by pathogen) and become activated
-T-cell receptors bind to antigen and activate helper T-cells to divide by mitosis to make large nos of clones

76
Q

what types of cell can activate an immune response

A
  1. phagocytes
  2. cancerous/abnormal cells
  3. transplanted cell/non-self cell
    4.cell invaded by a virus
77
Q

4 roles of helper T-cells

A
  1. activate B-cells
    2.stimulate more phagocytosis
  2. become memory cells
  3. become cytotoxic T-cells
78
Q

role of cytotoxic T-cells

A

-secrete 2 enzymes:
Perforin - forms pore in membrane of pathogen
Granzyme - enters through pore and activates enzymes that cause cell death

79
Q

what cells are involved in humoral immune response + where do they mature (brief)

A

-B-cells/lymphocytes
-mature in bone marrow and concentrate in lymph nodes and spleen

80
Q

role of B-cells

A

-when B-cell antibody (on surface) binds with specific complementary antigen, B-cell internalises the antigen and presents it on its surface
-T-helper cells then bind to presented antigen, causing B-cell to proliferate (clone) by mitosis (clonal expansion) into plasma cells and memory cells
-Plasma cells produce and release specific antibodies, which can coat pathogen, making it easier for phagocytes to engulf them, prevent pathogen entering a host cell or neutralise toxins produced by pathogen

81
Q

what is the primary immune response

A

-initial contact w pathogen antigen produces slow, small immune response
-not enough B-cells make the specific antibody needed
-person will show symptoms of infection

82
Q

what is the secondary immune response

A

-repeated exposure to antigen produces faster, larger immune response
-memory B-cells divide into plasma cells that produce the specific antibody
-memory T-cells divide into cytotoxic T-cells
-pathogen killed before any symptoms show

83
Q

what is active immunity (inc natural and artifical)

A

-requires exposure to antigen
-long term protection (memory cells produces)
-takes longer for protection to develop
Natural active: after catching a disease
Artificial active: after vaccination

84
Q

what is passive immunity (inc natural and artificial)

A

-doesnt require exposure to antigen
-short term, immediate protection (no memory cells produced)
Natural passive: baby receive antibodies through breastmilk/placenta
Artificial passive: blood transfusion including antibodies

85
Q

what is a vaccine (brief)

A

-an attenuated (weakened) or inactivated pathogen that stimulates an immune response

86
Q

how do vaccine lead to protection

A
  1. antigen on surface of pathogen bind to surface protein receptor on specific B-cell
  2. the now activated B-cell divides by mitosis to produce plasma cells (division stimulated by T-cells and cytokines)
  3. B-cells/plasma cells release antibodies
  4. some B-cells become memory cells that produce antibodies faster during secondary response
87
Q

what are live attenuated vaccines + features

A

-weakened pathogen multiplies slowly, allowing body to recognise antigens and produce primary immune response
-longer, stronger immune response
-unsuitable for ppl w immune deficiency
-eg. MMR vaccine

88
Q

what are inactivated/dead vaccines + features

A

-pathogen destroyed w heat/chemicals
-weaker immune response, requires boosters
-suitable for ppl w immune deficiency
-eg. Polio vaccine

89
Q

what is AIDS

A

-acquired immune deficiency syndrome
-T-cell levels drop below threshold so immune system becomes weakened as cannot produce large enough immune response due to B-cells not being activated
-means antibodies arent produced

90
Q

HIV structure

A

-two RNA strands, enzyme reverse transcriptase, capsid, lipid envelope, attachment proteins

91
Q

replication of HIV

A
  1. HIV enters bloodstream and attaches to CD4 protein on helper T-cells
    2.capsid fuses w CS membrane and RNA and enzyme from HIV can enter T-helper host cell
    3.enzyme reverse transcriptase turns viral RNA into DNA, which is moved to nucleus of host to be replicated
  2. replicated HIV breaks out of cell and piece of helper T-cell CS membrane forms its lipid envelope
92
Q

3 stages of HIV infection

A
  1. acute infection: lots of rep, symptoms of bad flu
    2.clinical latency: rep at very low rate, no symptoms
  2. AIDS: helper T-cell levels fall below threshold and weakened immune system can no longer respond effectively. vulnerable to other infections eg. meningitis, cancers
93
Q

uses of monoclonal antibodies

A
  1. pregnancy tests
  2. diagnosing HIV (ELISA testing)
  3. targeting cancer cells w drugs
  4. detecting cancer cells
94
Q

how MA work in pregnancy tests

A
  1. hCG binds to antibodies in test that are specific to hCG. antibodies are attached to coloured bead
    2.hCG-antibody complex moves down test and binds to immobilised antibody in test window. beads make colour show up
  2. control window has immobilised antibodies specific to mobile antibodies (that have coloured beads attached)
95
Q

2 types of ELISA tests + short explanation

A
  1. direct - use single antibody complementary to antigen being tested for
  2. indirect - use 2 different antibodies (pri and sec)
96
Q

indirect ELISA for antibodies (HIV)

A
  1. HIV antiGENS bound to bottom of vessel
    2.blood plasma added. if HIV antiBODIES present, they will bind to antigen
  2. wash out vessel
  3. add sec antibodies (specific to pri antibodies) w enzyme attached
  4. wash out vessel
  5. substrate added. if sec antibodies present due to pri antibodies being present, colour change will occur, indicating HIV positive
97
Q

indirect ELISA for antigens (prostate cancer)

A
  1. antiBODIES bound to bottom of vessel
    2.blood plasma added. if antiGENS present, they will bind to antibodies
  2. wash out vessel
  3. add sec antibodies (specific to pri antibodies) w enzyme attached
  4. wash out vessel
  5. substrate added. if antigens present, colour change will occur, indicating cancer positive