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Biology: lifes machinary > module 6: organisms adapting to change > Flashcards

module 6: organisms adapting to change Flashcards

(106 cards)

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1
Q

why are cold temperatures fatal human to organisms

A

Cold and freezing temperatures change concentrations of solutes and cause ice crystals to form, killing cells

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2
Q

why are hot temperature harmful to organisms

A
  • proteins begin to denatures
    -enzymes begin to denature
    -breaking their 3^o structure
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3
Q

what happens when you freeze a cell

A

· Ice forms outside of the cell (this can physically disrupt the cell, the phospholipid layer)
· Liquid water is lost from the cell to make up from the lack of liquid water outside of the cell
This tends to cause cells to die

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4
Q

how ca animals live in conditions where the tempreature is below 0 degrees

A
  • Anti-freeze proteins- organism makes these protein to interreact with the ice crystals to prevent them from getting too big, helps maintain water within the cell
    Have lots of solutes- serve to lower the temperature of water from freezing (about -2-3 degrees
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5
Q

how can taq polymerase live in hot temperatures

A

· Thermus aquaticus grows best at 65-70 degrees
· Enzymes optimised to function best at higher temperatures
DNA polymerase is not denatured at 95 degrees (it is stable at 94 degrees), stable and functional

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6
Q

what is taq polymerase used for

A

PCR

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7
Q

what are the steps for PCR

A
  1. Denature DNA - DNA is denatured to break the hydrogen bonds (94 degrees)
  2. Anneal the new DNA- primers are added to the DNAs (54 degrees)
  3. Extend- Taq polymerase synthesis a complimentary DNA molecule (72 degrees)
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8
Q

what is an exotherm

A

a type or organism that depends on the environment for their heat source (if its hot they will get hot and if it is cold they will be cold)

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9
Q

what is an endotherm

A

a type of organism that varys metabolic heat production, compensating for heat loss to the environment

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10
Q

what are disadvantages of being an endotherm

A
  • Requires more food consumptions
  • Inefficient energy use (ion leakage across membranes is less effective than in exotherms
    -Energy spend addressing this causes an increases in heat
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11
Q

what are the benefits of being endotherm

A
  • Presence in thermal niches inaccessible to exotherms (independence from environmental temp)
    • They can live in different environments
    • Higher muscle power and sustained activity
      -Protects against infection and disease (internal environment tends to be higher then the living environment for pathogenic bacteria)
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12
Q

what is allen’s rule

A

· A rule to that is used to be able to determine the environment of an organism
· It states that animals with smaller ears live in cooler environments whereas animals with larger ears live in warmer climates

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13
Q

what is an example of allens rule

A

· Ears become smaller and face become smaller to help conserve body heat
- The big ears are a way to radiate heat and loss heat more efficiently

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14
Q

what is bergmanns rule

A

· A rule to that is used to be able to determine the environment of an organism
It states that animals with smaller ears live in cooler environments whereas animals with larger ears live in warmer climates

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15
Q

what is an example of allens rule

A

peguims become larger as you get closer to the poles
Therefore smaller animals live near the equator

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16
Q

is the global temperature increase bad for humans

A

yes, because Increasing the average temperature of the planet brings microbes to temperatures more closely aligned to ours and therefore this means pathogenic bacteria may be able to survive in our body

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17
Q

why is increasing CO2 bad for organisms

A

The increase in CO2 is happening at a rate that animals, plants, and microbes cannot keep up with, posing a big challenge.

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18
Q

what are 2 plant mechanisms for the intake of CO2

A

-C4 pathway and the CAM pathway

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19
Q

where are C4 plants usually located

A

hot and dry places

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20
Q

how is water efficiency in C4 plants

A

-close stomata during the day
- reduced water loss through transpiration
-co2 is fixed into bundle sheath cells
-minimising water loss

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21
Q

how is photorespiration decreased in C4 plants

A
  • CO2 is concentrated in the bundle sheath cells which maintains a high concentration of Co2- this reduced the likelihood of rubisco favouring oxygen and losing the plant energy
    • Allow them to loss less energy as ATP and NADPH are not used in energy loss like photorespiration
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22
Q

what is the problem with rubisco

A
  • As temperature increases rubisco finds it hard to distinguish between Co2 and O2
    • Increases photorespiration
      Increases energy loss
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23
Q

what are the stages that occur in the mesophyll cells in C4 plants

A
  • CO2 enters through the stomata into the mesophyll cell
    • CO2 is converted into HCO3- (bicarbonate) which is catalysed by carbonic anhydrase (CA)

PEP carboxylase converts bicarbonate into oxaloacetate (OAA) which is then transported into the bundle sheath cells

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24
Q

what happens in the bundle sheath cell in C4 plants

A
  • OAA is transported into the bundle sheath cell
    • OAA is then decarboxylated releases CO2 at rubisco
    • this initiated the calvin cycle

A three carbon molecule (3-PGA) is transported into the mesophyll cell

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25
what is the CAM Process
-co2 intake -co2 concersion -storage -decarboxylation -calvin cycle
26
what happens in the CO2 intake stage for CAM plants, and what is the effect (time of day and result)
- Stomata opens during the night to allow CO2 to enter the cell This means less water escapes as it is colder during the night
27
what happens in the CO2 conversion stage for cam plants
- CO2 is then converted into a 4 carbon molecule by the enzyme PEPC This occurs in the mesophyll cells
28
what happens in the storgae stage for cam
► Storage - CO2 is stored as a C4 acid in the vacuole in the mesophyll cell This allows the plant to retain a high concentration of carbon until the day
29
what happens in the CO2 conversion stage for cam plants
- CO2 is then converted into a 4 carbon molecule by the enzyme PEPC This occurs in the mesophyll cells
30
what happens in the CO2 conversion stage for cam plants
- CO2 is then converted into a 4 carbon molecule by the enzyme PEPC This occurs in the mesophyll cells
31
what happens in the decarboylation stage for cam plants
- During the day the c4 molecule is decarboxylated which released CO2 and a C3 acid molecule The C3 acid molecule is used to then be converted into starch
32
what is the calvin cycle
process where CO2 is used to make glucose through -carbon fixation -reduction -regeneration
33
what is a pathogen
a disease causing microorganism
34
what is a disease
any condition which the normal structure or function of the body is damaged or impaired
35
what are the 3 stages of the immune system
1. recognition 2. activation 3. effector stage
36
what happens in step 1- recognition
a pathogen is reconsided as non self by by specialised receptors present in th cell
37
what are the receptors called what recognize self and non self antigens
they are called pattern recognition receptors (PRR receptors)
38
what are the 2 locations of the PRRs
1. cytoplasm 2. plasma membrane
39
where are TLRs found (toll like receptors)
in the cell membrane
40
what do TLRs detect
MAMPs and DAMPs
41
what is a MAMP
microbial associated molecular pattern
42
what organism express MAMPs
virus bacteria paracites
43
what molecules can MAMPs be
carbohydrates, poplypeptides or nucleic acids
44
what are DAMPs
damages associated molecular patterns
45
what dio DAMPs signal
-signal damgae to a cell when a pathogen damages it -Molecules released by stressed, dead or dying cells, signals of tissue damage
46
what is a PAMP
Pathogen associated molecular pattens
47
how does a PAMP arise
through the addition of a MAMP and DAMP
48
what happens when a PRR senors a PAMP
1. Secretion of defensive or antimicrobial peptides 2. Production of pro-inflammatory cytokines 3. Activation of compliment system 4. Phagocytosis - All of these steps are non specific
49
what are defensins
- an ancient defense mechanism where positively charged polypeptides disrupt the phospholipid bilayer of a pathogen killing the pathogen
50
how do defensins work
The positive defensin (positive polypeptide) and negative phosphate (phosphate head) collide due to the opposite charges
51
what is phagocytosis
the process why which a cell engulfs large particles in a phagocytic vacuole (phagosome) and engulfs them
52
when does phagocytosis occur
Once the pathogen have been disrupted or identified they must be removed from the cell
53
what cells undergo phagocytosis
dendritics cells macrophages
54
what occurs after phagocytosis
1. more immune cells come to the site 2. antigen is presented to b and t cells (adaptive immunity)
55
where do b cells mature
in the bone marrow
56
what are 2 types of b cells
- plasma cells - b memory cells
57
where are t cells matured
in the thymus
58
what are the 3 types of t cells
CT t cells TH cells t memory cells
59
what is the process the production of t cells
* Phagocyte (macrophage or dendrtic cell) present antigen to the t cell- this causes the t cell to become activated * Then the t cell will proliferate (make lots of them) * Differentiate into - CTs- kill the pathogen -Th cell- release cytokines that signal to other immune cells to kill the pathogen
60
what is the process of producing b cells
-phagocyte presents antigen to naive b cells - the antigen is broken down into polypeptides and is displayed on the surface of the naive b cell through a MHC 11 - a T helper cell then binds to the polypeptide and the the naive b cell becomes activated - this causes the b cell to proliferate and undergo cell division -this produces memory b cells and plasma cells which secrete antibodies
61
what genes in the heavy chain code for antibodies
V region J region and the D region
62
how do antibodies change to be specific to antibody
through VDJ recombination
63
what is the result of VDJ recombination
diversity of antibodies
64
how do plant deal with pathogens
-secrete toxic molecules to program cell death - have structural barriers- bark and cell walls
65
how many types of organisms cause disease
10
66
what are virus
us · Infectious agent · Not cellular · Cannot replicated by itself · Needs a host cell to make copies of itself · Comprised of a genome, protein and sometimes a membrane · No ribosomes, organelles, energy metabolism · They are very small (nm) Most viruses are plant pathogens
67
what are some viral dieases
HIV MERS COVID19
68
why are virus hard to treat
· Virus can be difficult to treat because the use of the host cellular machinery for replication
69
how do pathogens cause harm to hosts
1. Consumption 2. Grows in the host 3. Invades the hosts immune system and defence 4. Damage the host - taking away resources, physically destroying cells Leave the host and start the circle again
70
what is mutalism
When host and microbe both benefit off each other
71
what is commensalism
Causes no harm or no benefit to either the host or microbe
72
what is parasitism
When the microbe benefits to the expense of the host, often the cause for pathogens
73
what is a primary pathogen
Cause overt, immediate disease in most healthy people
74
what is an oppotunistic pathogen
Cause disease only if immune system is weakened
75
what happens to the host if a pathogen is virulent
-ususally more danagerous as the pathogen will not be spread because the host is in bed
76
what is the red queen hypothesis
· Host and pathogens are constantly trying to outsmart each other · One thrives at the expense of the other The host are interested in defending against the pathogen Their interests are endless as they both evolve to try and avoid disease
77
how do bacteria become resistant to antibiotics
· Bacteria have specific genes to break down antibiotics, often carried on small pieces of DNA (plasmids) · These plasmids or fragments of DNA can be moved between species · This is down through horizontal gene transfer Therefore if a plasmid if resistance it can be shared really easily between bacteria
78
how do antimicrobial chemicals work
-work by inhibiting the microbes biochemical processes, thereby stopping the spread of the pathogen in the host
79
what are the 3 types of cancer
- Hereditary cancers - Sporadic (non hereditary cancers -Transmissible cancers
80
what is a tumour
· A tumour is a mass of cells
81
what is a bengin tumour
· Benign tumours do not have the ability to invade other tissues a mass of cells that do not have the ability to invade other cells
82
how are herditary cancer passed on
Genes can be inherited that are cancerous which is passed onto the new generation
83
what are the 2 types of cancer genes
1. Tumour suppressor genes 2. Dominate oncogenes
84
what do tumour suppressor genes do
helps control cell growth
85
what does a dominate mutation do
they gain a function
86
what does a recessive mutation do
loss a function
87
proto-oncogenes generally become....
oncogenes in a dominant manner
88
do tumour suppressors have roles in cell cycle, and how
yes, they are involved in the DNA damage detection
89
what is simulated when DNA damage is detected
tumour suppressor stimulates the production of p21
90
what does p21 do
binds to G1 CDKs which prevent their activation and stops the cell cycle
91
what is one type of recessive tumour suppressor
p53
92
what does p53 do
sensors DNA damage
93
what happens with the p53 in 50% of all cancer
it gets mutated and losses its function
94
what happens when p53 is working normally
- DNA is damaged and p53 is activated and binds to area - Cell halts at g1 checkpoint - DNA repair is activated and apoptosis is triggered if not repairable - Cells don’t pass on damaged DNA
95
what happens when p53 is not working properly
- DNA is damaged and cannot bind to area - Cell cycle is progessed (this is bad) Damaged DNA (mutations) are passed on
96
what is RAS
a proto-oncogene that is mutated in many cancers - responsible for cell division and proliferation
97
what happens when RAS is not cancerous
normal cell division and proliferation as - growth factor receptor binds onto ras
98
what happens when RAS is cancerous
-RAS is always on and is dividing cells and proliferating them even when the grow receptor is not binded - this is cancerous (cell growth)
99
what is peto's paradox
large animals are made up of lots of cells and therefore should get cancer more than smaller organisms but this is not true
100
why dont elephants get cancer as much as mice
because they have 20 copies of the p53 gene, therefore it is much more liekly that a mutation will damage 2 alleles then all 40 alleles
101
what is an example of a transmissable cancer
tasmanian devils cancer which killed up to 80% of all devils
102
how did the devils get the cancer
· Most likely spread between animals biting each other faces during fighting · The microbes invade the hosts immune system · These microbes infect cells and hijack the cellular machinery causing cells to proliferate and become cancerous
103
why does cancer affect older generations
Because developing cancer requires accumulating multiple mutations which takes time
104
is always cancer genetic
no, there are environmental factors that can cause cancer like smoking
105
why is burning crops good
thins out the young shrubs and trees while preserving the canopy and encourages growth of new grass
106
what is domestication
involes one species that controls the reproduction and breeding of second species

Biology: lifes machinary (7 decks)

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