cells2 Flashcards

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1
Q

List stages of mitosis.

A
Interphase
Prophase
Metaphase
Anaphase
Telophase
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2
Q

Outline Interphase.

A

Precedes Mitosis

  1. Cell is not dividing.
  2. Considerable cellular activity - replication of DNA, two copies on centromere.
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3
Q

Outline Prophase.

A
  1. Chromosomes become more visible, thicken.
  2. Centrioles move to opposite ends of the cell (poles).
  3. Spindle fibres develop from each of the centrioles (spindle apparatus).

NB = plants lack centrioles, but are not essential as they still have the spindle apparatus.

  1. Nucleolus disappears and the nuclear envelope breaks down, leaving the chromosomes free in cell cytoplasm.
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4
Q

Outline Metaphase.

A
  1. Chromosomes seen to be made up of two chromatids.

2. Microtubules attach to centromere - chromosomes pulled to the cell equator where they line up.

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5
Q

Outline Anaphase.

A
  1. Centromeres divide, separating each pair of sister chromatids.
  2. Chromatids pulled to their respective poles as spindles contract, centromeres first - v-shaped.

NB =
Mitochondria provide energy; gather around spindle.
Mitosis can be prevented by introducing spindle-destroying chemicals.

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6
Q

Outline Telophase.

A
  1. Chromosomes reach their respective poles and then uncoil, become long and thin again - chromosomes again.
  2. Spindle fibres disintegrate; nuclear envelope and nucleolus reform.
  3. Cytoplasm divides in cytokinesis.
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7
Q

Outline how viruses replicate.

A

Acellular, non-living, so do not undergo cell division.

  1. Attach to host cell with the attachment proteins on their surface.
  2. Inject nucleic acid into host cell.
  3. Viral nucleic acid then hijacks the cell’s machinery and codes for metabolic processes to produce viral components - nucleic acid, enzymes, structural proteins, which are then assembled into new viruses.
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8
Q

Why is mitosis so important? Outline 3 reasons.

A
  1. Growth - ensures that all cells growing from original cell of an organism are genetically identical.
  2. Repair - Important that replacement cells produced have an identical structure and function to lost cells.
  3. Reproduction - Single-celled organisms divide by mitosis to give 2 new organisms - each new organism is genetically identical to the parent organism.
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9
Q

Mitotic Index - equation.

A

Mitotic index = number of cells undergoing mitosis (cells with visible chromosomes) / total number of cells in field of view.

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10
Q

Outline the stages of the cell cycle.

A

cycle.
G1 - cell grows, new organelles and proteins made.
S - synthesis - DNA replication.
G2 - cell keeps growing and proteins needed for cell division are made.
Mitosis.
Cytokinesis.

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11
Q

How does cancer arise? Difference between benign and malignant?

A

Result of gene damage controlling mitosis and cell cycle.

Mutant cells are structurally and functionally different - most mutant cells die but surviving mutant cells become tumours.

Malignant - grow rapidly, less compact, more likely to be life-threatening.
Benign - grow more slowly, more compact, less likely to be life-threatening.

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12
Q

How can cancer be treated?

A

Involves killing dividing cells by blocking a part of the cell cycle - cell division and therefore cancer growth ceases.

Chemo disrupts cell cycle by preventing DNA replication or by inhibiting the metaphase stage of mitosis by interfering with spindle formation.

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13
Q

Suggest why we don’t use larger or more frequent doses to kill more cancer cells.

A

Not given more frequently because healthy cells would not be able to increase their numbers to near normal again between treatments - numbers would decline more rapidly and possibly kill the patient.

Not in higher doses because even more healthy cells killed each time…(same as above).

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14
Q

Outline role of phospholipids in cell-surface membrane structure.

A

Their hydrophilic/hydrophobic interactions lead to the formation of a phospholipid bilayer.

  1. Allow lipid-soluble substances to enter/exit cell.
  2. Prevent water-soluble substances entering and leaving cell.
  3. Make the membrane flexible and self-sealing.
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15
Q

Outline role of proteins in cell-surface membrane structure.

A

Some in surface of bilayer:

  1. Act to provide mechanical support to membrane.
  2. Along with glycolipids, act as cell receptors for molecules such as hormones.

Some span the entire membrane:

  1. Protein channels - water filled tubes allowing water-soluble ions to diffuse across the membrane.
  2. Protein carriers - bind to ions or molecules like glucose/amino acids - then change shape to move these molecules across the membrane.

-

  1. Help cells adhere together.
  2. Form cell-surface receptors for identifying cells.
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16
Q

Outline role of cholesterol in cell-surface membrane structure.

A

Within the phospholipid bilayer of cell-surface membranes:

  1. Reduce lateral movement of other molecules (including phospholipids) - pulls together the fatty acid tails, limiting movement without making the membrane too rigid.
  2. Make the membrane less fluid at high temperatures.
  3. Prevent leakage of water and dissolved ions from the cell, as cholesterol molecules are very hydrophobic.
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17
Q

Outline role of glycolipids in cell-surface membrane structure.

A

Carbohydrate covalently bonded to a lipid in the membrane:

  1. Carbohydrate portion extends from the phospholipid bilayer into the watery environment outside the cell - there acts as a cell-surface receptor for specific chemicals (ABO blood system)
  2. Help maintain the stability of the membrane.
  3. Help cells to attach to one another and so form tissues.
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18
Q

Outline role of glycoproteins in cell-surface membrane structure.

A

Carbohydrate chains attached to many proteins on the outer surface of the cell-surface membrane.

  1. Cell-surface receptors for hormones and neurotransmitters.
  2. Help cells to attach to one another and so form tissues.
  3. Allow cells to recognise one another - lymphocytes can recognise an organism’s own cells.
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19
Q

Comment on the permeability of the cell-surface membrane.

A

Controls the movement of substances into/out of the cell.

Most molecules don’t freely diffuse across it because many are:

  1. Not lipid-soluble
  2. Too large to pass through
  3. Same charge as protein channel charges - repelled even if small
  4. Charged/polar - can’t pass through the non-polar hydrophobic tails in the phospholipid bilayer.
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20
Q

Explain the “fluid-mosaic” model of the cell-surface membrane structure.

A

= arrangement of all the various molecules combined into the structure.

Fluid = membrane is flexible and can constantly change in shape as individual phospholipid molecules can move relative to one another.

Mosaic = Proteins embedded in the phospholipid bilayer vary in shape, size + pattern like tiles in a mosaic.

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21
Q

Define diffusion.

Give the equation for Fick’s Law.

A

= The net movement of molecules/ions/particles from a region of higher concentration to a region of lower concentration.

Fick’s Law:

diffusion rate = (SA x gradient x permeability) / (membrane thickness).

22
Q

Define facilitated diffusion.

Comment on the roles of the proteins involved in facilitated diffusion.

A

Movement of larger/charged/polar species made easier by protein channels/carriers that span the membrane.

NB=Passive process, only difference is that fd occurs at specific points on the plasma membrane where there are protein molecules.

Channel Proteins = Water-filled hydrophilic channels allowing specific water-soluble ions to pass through - selective channels - only open when specific ion binds to protein causing it to change shape -> open and closed on different sides of the membrane.

Carrier Proteins = Molecule specific to the protein binds, changes shape of protein -> molecule released to the inside of the membrane.

23
Q

Define osmosis.

A

The net passage of water molecules from a region of higher water potential to a region of lower water potential across a selectively permeable membrane.

24
Q

Comment on water potential.

Define haemolysis.

Define plasmolysis.

A

= Pressure created by water molecules.

Addition of water will lower wp.
wp = 0 when pure water at 298K, standard conditions.

Water will move towards the area of lowest wp by osmosis, until an equilibrium is established.

Haemolysis = rupture of RBC cell-surface membrane due to water entering by osmosis.

Plasmolysis = Shrinking of RBC -> water leaving by osmosis -> darker appearance of RBC due to increased haemoglobin concentration.

25
Q

Comment on osmosis in plant cells when water moves in/out.

A

Protoplast (cell parts within cell wall) pushes on cell wall when swells - turgid.

If water leaves by osmosis, point is reached where protoplast no longer presses on cellulose cell wall - incipient plasmolysis.

Further loss of water by osmosis -> cell contents shrink further and protoplast pulls away from cell wall - cell is said to be plasmolysed.

26
Q

Define active transport.

A

Movement of particles into/out of a cell from a region of lower concentration to a region of higher concentration using ATP and carrier proteins.

27
Q

Outline how active transport takes place.

A
  1. Molecules bind to carrier protein and ATP attaches to the membrane protein on the inside of cell/organelle.
  2. Binding of phosphate ion to protein changes shape, allowing access for molecules to inside of the membrane but closed to the outside.
28
Q

Comment on the relationship between Fick’s Law and the adaptations of specialised cells.

A

Specialised cells will have different surface areas, numbers of channel/carrier proteins, differences in concentration gradients/ wp —- all to increase or decrease the rate of movement across cell membranes.

–> think how permeability affected by numbers of proteins in a given area etc. - relate to fick’s law.

29
Q

Outline the process of Co-transport in the ileum.

A
  1. Na+ actively transported out of epithelial cells into blood via Na+/K+ pumps (carrier molecules in epithelial cell-surface membrane).
  2. Increased Na+ conc maintained in lumen of intestine than in epithelial cells.
  3. Na+ diffuse into epithelial cells down Na+ gradient through a co-transport protein —> carrying glucose (/amino acids) with them.
  4. Glucose/amino acids pass into the blood plasma by facilitated diffusion using another type of carrier, against their conc gradient.

=> Indirect active transport - as [Na+] gradient provides energy for process, not ATP - but ATP needed for 1.

30
Q

Comment on the significance of proteins on the cell surface in regards to recognition.

A

Protein molecules on the cell-surface membrane enable the immune system to identify:

  1. Pathogens.
  2. Cells from other organisms of the same species - non-self material (different genes).
  3. Toxins (produced by pathogens - leads to chemotaxis)
  4. Abnormal body cells - such as cancer cells.
31
Q

Define clonal selection.

Comment on the existence of specific lymphocytes before immune response.

A

= Stimulation of (B) lymphocytes to undergo rapid mitotic division to produce B-plasma cells after having been activated (by TH-Cells).

-> clonal selection explains the time-lag between exposure and bringing it under control.

Specific lymphocytes already exist- high probability that one of the millions of different lymphocytes will have a complementary protein to an antigen.

32
Q

List main defence mechanisms.

A
  1. Physical and Chemical barriers - skin.
  2. Non-specific - phagocytes.
  3. Cell-mediated (specific).
  4. Humoral (specific).
33
Q

Why is infection in the foetus rare?

A

Because it is protected from the outside world by the mother and the placenta.

34
Q

What happens in regards to lymphocytes with receptors complementary to normal body cell antigens?

A

In the foetus, they are either suppressed or killed off.

  • undergo programmed cell death (apoptosis).

=> only lymphocytes with receptors complementary to non-self antigens remain in the blood.

35
Q

Outline the process of phagocytosis.

A
  1. Chemotaxis of phagocyte to pathogen as pathogen produces toxins and other materials. Phagocyte moves towards pathogen down concentration gradient.
  2. Receptors on phagocyte surface attach to chemicals on pathogen surface.
  3. Vesicle/Phagosome forms, engulfing the pathogen, and lysosomes migrate towards the vesicle.
  4. Lysosomes release lysozymes into the vesicle, where they destroy the pathogen by hydrolysis.
  5. Hydrolysis products of the bacterium/pathogen are absorbed by the phagocyte.
36
Q

Define antigen.

A

(foreign) Protein on the surface of a pathogen that stimulates an immune response.

NB=> toxins can also act as antigens.

37
Q

Comment on antigenic variability and its effect on vaccines.

A

Memory Cells from primary immune response do not recognise the different antigens as they are immunologically distinct.
=> no secondary response - primary response again so takes time to get ill again.

Influenza vaccine changes yearly -> new immunologically distinct strains not recognised by memory cells circulate in population.
=> most suitable vaccine implemented in a vaccination programme.

38
Q

Define immunity.

A

The ability of organisms to resist infection by protecting against disease-causing microorganisms or their toxins, that invade their bodies.

39
Q

Which type of cells are most involved with cell-mediated immunity? Where do they mature?

A

T-cells, which mature in the thymus gland.

40
Q

Define cell-mediated immunity.

A

T-lymphocytes respond only to antigens that are presented on a body cell, rather than antigens in the body’s humour (fluids).

41
Q

T-lymphocytes can distinguish antigen-presenting cells from normal cells, as:

A
  1. Phagocytes that have hydrolysed pathogen present its antigens on their own cell-surface membrane.
  2. Body cells invaded by a virus present some of the viral antigens on their own cell-surface membrane.
  3. Transplanted cells have different antigens on their cell-surface membranes.
  4. Cancer cells are different from normal body cells and present antigens on their own cell-surface membranes.
42
Q

Define antigen-presenting cell.

A

= Cells that display foreign antigens on their surface.

43
Q

Comment on the specificity of T-cells.

A

Receptors on each T-cell are complementary to, and respond to only one antigen.

There are a vast number of different T-cells with each one responding to a different antigen.

44
Q

Outline the process of cell-mediated immunity.

A
  1. Pathogens invade body cells/taken in by phagocytes.
  2. Phagocyte places pathogen’s antigens on its own cell-surface membrane.
  3. Receptors on specific Th-Cell complementary to this antigen.
  4. Attachment activates rapid T-cell division by mitosis, to form clones of genetically identical cells.
  5. Cloned T-Cells:
    a) stimulate phagocytes to engulf pathogens by phagocytosis.
    b) activate Tc-Cells which produce perforin protein which make pathogen membrane freely permeable.
    c) develop into memory cells, enabling a rapid secondary immune response to future infections by the same pathogen.
    d) stimulate clonal selection of B-Cells and stimulate them to secrete their antibody.
45
Q

T-cell action is most effective against which type of pathogen? Why?

A

Most effective against viruses, as they need host cells to survive and replicate.

46
Q

Define humoral immunity.

A

= Involves B-cells and antibodies, soluble in blood and tissue fluids of body - B-cells produce specific antibodies, specific to one antigen.

47
Q

Which type of cells are most involved with humoral immunity? Where do they mature?

A

B-cells.

Bone marrow.

48
Q

What are plasma cells?

A

= Secrete antibodies (usually) into blood plasma, only survive for a few days - lead to destruction of pathogen.

49
Q

What are memory cells?

A

= Circulate in blood and tissue fluid - divide rapidly into plasma cells and more memory cells -> more antibodies at a faster rate (faster response).

=> provide long-term immunity - we are often unaware if we are reinfected.

50
Q

Outline the process of humoral immunity.

A
  1. Surface antigens of an invading pathogen are taken up by a B-cell.
  2. B-cell processes antigens and presents them on its surface.
  3. Th-cells (activated earlier) attach to the processed antigens on the B-cell and activate it.
  4. B-cell is now activated to divide by mitosis to give a clone of plasma cells.
  5. Cloned plasma cells produce monoclonal antibody and secrete it; antibody exactly complementary to antigen on pathogen’s surface.
  6. Antibody attaches to antigens on the pathogen + destroys them by marking them for phagocytosis.
  7. Some B-cells then develop into memory cells, circulating in blood.