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Genes and Environment > W4 > Flashcards

W4 Flashcards

1
Q

describe the transformation of a normal cell to a sickle cell

A
  • mutant haemoglobin beta subunit
  • caused by a mis sense mutation

DNA code:
- A becomes T in primary strand and T becomes A in secondary strand.

mRNA:
- A becomes U

amino acid:

  • 6th place
  • Glutamic acid becomes valine

a normal functioning RBC now has rapid deoxygenation in tissues

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2
Q

describe sickle cell mutants in terms of what happens when a person has 1HBS and 2HBS

A

1HBS:

  • decreased growth
  • delayed sexual maturity
  • impaired mental function
  • impaired infection resistance
  • increased chance of stroke, kidney failure, pneumonia, osteomyelitis, bone deformity, jaundice and heart failure

2HBS:
- die at birth usually

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3
Q

describe survival from genotypes in areas without malaria

A
  1. if a heterozygous sickle cell parent HBS/HBA and a homozygous normal parent 2HBA have a baby, then of the 4 possible baby types, 2 are HBA/HBA and 2 are HBS/HBA
  2. if both parents are HBS/HBA, of the four possibilities, 1 is HBA/HBA, 2 are HBS/HBA, 1 is HBS/HBS and this dies before reproducing
  3. If both parents are HBA, all four possibilities are HBA and should survive to reproduce
  4. HBS/HBA babies will also survive and reproduce less, so the HBS allele will become less common, but these tend to survive malaria
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4
Q

describe survival from genotypes in areas with malaria

A
  1. most babies of HBA/HBA parents will like die of malaria
  2. if one parent is HBS/HBA, and one parent is HBA/HBA, of the four possibilities for the baby, 2 are HBA/HBA and 2 are HBS/HBA. the two HBS/HBA may survive malaria
  3. if both parents are HBS/HBA, then of the 4 possibilities, 2 are HBS/HBA and 1 is HBS/HBS and this dies before reproducing and 1 is HBA/HBA who is likely to die of malaria
  4. HBS/HBA babies would survive and reproduce more when they become parents, so HBS allele becomes more common
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5
Q

what is the definition of allele, mutation, homozygote, heterozygote and polygenic variation

A

allele: version of gene
mutation: chance in a gene leading to new allele
homozygote: alleles from father and mother are the same
heterozygote: inherited alleles differ
polygenic variation: many genes combine to determine a characteristic

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6
Q

how does one describe evolution due to natural selection

A

if individuals vary in how well they cope with their environment, the relevant characteristics are heritable, then, those that cope well produce more offspring that survive to reproduce than those that do not cope, also, the proportion in the population with these characteristics increases. note: population chance, not individual

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7
Q

describe the steps in evolution of resistance to pesticides

A
  1. before pesticide is used, resistant mutants are rare
  2. doses decay over time, who will die and when
  3. when resistance first appears
  4. when resistance become common
  5. minimising selection for resistance
  6. mutation side effects and stabilisation of resistance
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8
Q

describe what happens in evolution of resistance to pesticides before a pesticide is used

A
  • very few mozzies may have mutant resistant allele ( R) by chance
  • there will be very few R and many with normals
  • so every resistant will likely mate with normals
  • they will produce half heterozygous resistants and half homozygous normals
  • almost no chance that two R will be in the same individual so no homozygous R
  • thus, every R will be heterozygote
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9
Q

describe what happens in evolution of resistance to pesticides when doses decay

A
  • the pesticide sprayed is always concentrated
  • it lands on surfaces mixes with dust and water so it becomes diluted over time
  • the dose a mozzie gets depends on when it lands on sprayed surface
  • adult mosquitoes in the sprayed area die
  • larvae in ponds, or eggs will hatch out later- all these die if they become adults too soon
  • other adults will fly in from the edges of the area
  • some, by chance may have a R
  • if they arrive after the dose has decayed enough, then R survive, while normals die. THIS IS SELECTION
  • if they arrive after the dose has decayed to very low levels, then both normals and few R survive, SO THERE IS NO SELECTION

EG. In hospital: if the infections can spread, patients may be reinfected while a dose is decaying

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10
Q

describe what happens in evolution of resistance to pesticides when resistance appears

A
  • graph lines stay the same, however, there is now a zone of selection and a selection time
  • while the doses decays through the zone of selection: it kills normals and leaves R, so the percentage of R increases. THIS IS SELECTION FOR RESISTANCE
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11
Q

describe what happens in evolution of resistance to pesticides when resistance becomes common

A
  • the line at which homozygotes survive appear.
  • the selection time increases
  • the zone of selection widens
  • heterozygote R may mate with other heterozygote R
  • produces homozygote R
  • these have higher resistance as most genes have incomplete dominance (heterozygote shows intermediate characateristics as neither of the alleles are dominant)
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12
Q

how can we minimise selection for resistance

A
  • repeat regularly high dosages ie. complete courses of drugs
  • don’t delay until pest returns, repeat doses at short intervals
  • use chemicals with rapid decays, this minimises selection time during decay
  • prevent unnecessary use
  • prevent dispersion of resistant pests, this prevents transfer to other patients
  • minimise edge effects for pesticides
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13
Q

describe edge effects

A

areas can either be sprayed one field at a time or a largee area once

  • in a large area, much of it is far from the edges. therefore, you kill the pests in the area and pests moving in will only get to edge areas as the dose decays
  • there is only one time when the dose is in the selection zone
  • if small areas are sprayed one by one, pests can move from area to area each spray while the dose decays
  • then selected resistant pests can move to areas sprayed later as doses decay there
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14
Q

what are the side effects of mutations

A
  • new mutations have bad side effects, otherwise the R alleles would be common already and another toxin would have to be used
  • therefore, after the dose is gone, they are selected against, unless the pesticide returns
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15
Q

what happens if the pesticide returns again after resistance was already developed

A
  1. resistance increases very quickly and there will be a high no. of homozygous resistant already present
  2. polygenic variation where some genes modify the effect of other genes, new gene combinations result from sexual reproduction lion in animals, in bacteria: new combinations arise from conjugation, transposons or plasmids. so genes that reduce side effects of resistance mutation may be combined with the R allele
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16
Q

describe stabilisation of resistance

A
  • if the pesticide is used after resistance becomes common then the:
  • mutant R allele must be retained
  • selection acts on combinations of R with other genes, to modify bad side effects
  • result is resistance with reduced side effects
  • this process involves polygenic variation- gene combinations
  • resistance will remain when pesticide use stops

THEREFORE: WE SHOULD STOP PESTICIDE USE ONCE RESISTANCE DETECTED

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17
Q

describe cross resistance

A
  • toxins target key insect physiology
  • many toxins act in similar ways
  • restart genes act against similar toxins
  • if similar toxins used: pests already partly resistant and resistance builds rapidly ie. polygenic process
    WE MUST SWTICH TO OTHER UNRELATED CHEMCIALS. LOTS OF MONEY THO
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18
Q

describe ecological effects of resistance

A
  • before resistance, pesticide reduces pest
  • spray will also kill many of other animals like predators and parasites
  • after resistance, spray has little effect on pest. leading to pest number increasing
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19
Q

describe with reference to an example of mites present on the human body

A
  1. demoted:
    - harmless commensal
    - common on everyone
  2. sarcoptes
    - an ectoparasite
    - itch mite: causes scabies
    - forms channels, red lines on the skin, very itchy
    What can we do?
    - poison for mites to kill them off, not very successful living on humans. selection rewards symbionts that don’t harm the host
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20
Q

explain how responses to symbionts can vary

A

depends on the type of symbiont (organisms living together)

commensal: symbiont that benefits and does not harm the other
parasite: symbionts that benefit and harms the other partner
muralists: symbionts that both benefit each other

  1. hosts resist harmful invasions by parasites eg. for the itch mite, we would seek advice and get a mite killing shampoo. the more harmful, the more we will try to eliminate it
  2. commensals are tolerated. eg. we are often not aware of demoted, so there are more demoted in the world then humans
21
Q

describe host parasite evolution

A
  1. under normal conditions, virulence is reduced ie. parasites become commensal and then become muralists
  2. parasites evolve to be less harmful:
    A. a parasite is not transferred if the host is killed rapidly
    B. the parasite benefits if the host is abundant
    C. hosts react most strongly to harmful parasites
  3. hosts evolve to be resistant: resistant hosts reproduce more
22
Q

describe with reference to an example what symbionts are preset on the human body and how their presence is good or bad

A
  • all gut and skin surfaces are covered by bacteria
  • there are almost no bacteria free areas eg. eyes, lung and bladder
  • our skin is only a partial barrier. but the IS is the major defence. but the lesions of the skin allow a flood of bacteria
  • our skin, gut e.t.c encourage particular bacteria. health refers to the natural balance of these bacteria. diseases results from disturbances to this balance, rather than the colonisation of new bacteria
23
Q

describe the three types of common gut bacteria and the role they play in the human body

A
  1. harmless parasites: use some of our food in gut
  2. commensals: eat compounds we cannot digest
  3. muralists:
    - partly digest food so we can then absorb it. - — some manufacture B and K group vitamins.
    - some produce other useful compounds like stimulate the immune system
    - some feed on harmful excretions of other bacteria
24
Q

describe babies and bacteria

A
  1. birth is the first contact with bacteria:
    - this is where the antibody system must start
    - it is important that pathogens are low or absent
  2. Bifidus bacteria on vagina, nipples of lactating women
    - ensures the baby gets bifidus
    - bifidus protects by decreasing the bacteria
  3. tasting behaviour of babies:
    - ensures full bacterial community
    - stimulates crossover immunities
25
Q

why do so many harmful parasites exist?

A
  1. they invade us by accident-
    - zoonoses: belong to other hosts
    - most common zoonoses are passed through shared ectoparasites/shared environments
  2. on co-evolved hosts, these parasites are fairly harmless
    - the crossover is often bad for the parasite too
    - therefore, there may be rapid evolution to exploit the new host
    - human-human transmission is rare until a parasite evolves
26
Q

describe the bubonic plague in terms of the spread and what causes the disease

A

Yestina pestis- bacterium
- fever, buboes, prostration, delirium, blackened skin and death

  1. vectors: fleas
    - ball of bacteria- blockage in flea’s gut
    - flea hungry, looks for new host
    - sucks harder, fails, recoil shoots bacteria into bite wound
  2. human coughing, transmits bacterium directly
27
Q

describe the life cycle of the bubonic plague and how it is relevant today

A
  • a zoonosis
  • normally a mild disease of wild rodents
    1. wild rodents: gerbil are the reservoir of the pathogens and it can transmit to other gerbil, black rats and humans via their fleas
    2. black rats can transmit their fleas to the black rats and humans
    3. humans can transmit their fleas to other humans

there are wild carriers of the plague currently in small random sections of the world such as Africa

28
Q

describe the dangers of rabies

A
  • once most of the most feared diseases
  • once symptoms develop, patient always dies
  • large RNA virus, specific to nerves
  • reservoirs in resistant foxes, racoons, bats: in Europe and USA especially
  • passes to dogs, then humans
  • red fox now common in Australia
  • this presents an enormous risk of rabies invasion
29
Q

outline and explain the risk that exotic zoonoses will enter Australia

A

risk factors:

  • animal hosts/vectors are in asutralia
  • hosts live close to humans
  • disease incubation period long

examples:
rabies- red fox common in Australian cities and this is close to us and our dogs
korean hemorrhagic fever which is a virus in rats and spread via urine
yellow fever through mosquitoes in Australia- spreading south with climate change

30
Q

list some of the exotic bioinvasions occurring now

A

tiger mozzie from SE Asia, cane blight from s. Asia

note: historically, there were cane toads and rats that caused wildlife devastation and acted as disease vectors/predators

31
Q

what affects the spread of disease

A
  1. density and movement of hosts:
    - high density=greater contact between individuals.
    - also, more movement=more contact between individuals
  2. size of host population where disease needs ongoing supply of susceptible individuals eg. need 500,000 to sustain measles
  3. nutritional and knowledge status of host population:
    - lack of protein can impair immune function,
    - micronutrients such as vitamin c and zinc are essential for immune function.
    - also, public understanding of how to avoid infection
32
Q

how fast do diseases spread?

A
  1. depends on transmission between hosts where there can be horizontal (between individuals or via vector or intermediate host) and vertical (between generations such as mother and child) transmission
  2. through networks such as hubs which foster lots of contacts
33
Q

describe the rate of spread of a disease

A
  • an epidemic occurs if the no. of infected increases exponentially
  • in a no. of infected vs time graph, the rate of spread at a given time is the slope. where the slope=r*N

it follows the r=PCD. where P is the probability of passing on disease, C- effective average number of contacts per year, D is the duration of infectiousness

epidemic if r>1

34
Q

outline what occurs when there is zoonoses and a disrupted ecology in reference to two examples

A

eg. logging for agriculture and development
- brings humans Into contact with new hosts and parasites
- contacts between domestic and wild animals
- increases nutritional stress in wild populations
- greater chance of spreading any native pathogens

US hillside forest

  • people moved into wooded hills in New England, USA
  • they drove bears and wolves out. thus the deer increased
  • deer ticks bit people, vectors for Lyme disease bacterium
35
Q

how can we achieve bio awareness?

A
  • reduce bio pollution ie. keep exotics out with quanrantine
  • immunisation of ourselves and poorer countries
  • public health measures in all countries, 30m people die per year of contained water
  • problems of more food from less area, denser population, we need better control of pests and diseases
  • minimise evolution of resistance
  • anticipate effect of climate chance eg. more sanitation disasters and more malaria in Aus
  • expand bio control research
36
Q

describe drug design to combat resistance

A
  • understand the molecular action of current antibiotics can aid rational drug design
  • most antibiotics target the bacterial ribosome
  • drugs can be designed to attack it, or even perhaps specific bacteria
37
Q

what factors need to be considered when making a pesticide or drug?

A
  • must be toxic to the pest/ parasite
  • must be harmless to us and domestic animals
  • must target some metabolic difference eg. bacterial ribosomes or membranes which are different from eukaryotes
    HOWEVER:
  • harder if the parasite is more like us
38
Q

describe an example of combating resistance in malaria

A
  • in the 1950s, Chloroquin resistant plasmodium was discovered, this is an enzyme that pumps out of a vacuoles in the parasite cell
  • a single gene was found to be responsible on chromosome 7
  • we need to design a drug to block it

the CRT enzyme pumps out chloroquine

39
Q

what must we consider when using biological knowledge to target parasites

A

what is the lifecycle

  • weak points
  • predators
  • parasites

can you encourage them
can you introduce new ones

40
Q

in reference to the ecology of mosquitoes, describe how you could target them

A

since we know that:

  • they plato eggs on the surface of water
  • larvae in pond
  • have some hydrophobic hairs to push water away when they attach to the water

so:

  • oil on surface of water to repel function of hydrophobic hairs
  • drain swamps
  • use BT: this is a bacteria predator
41
Q

describe how hormonal control can be used in insects that use moulting

A

Molting hormone:

  • constant at each moult
  • induces growth of new cuticle
  • begins melting process where there is partial absorption of old cuticle and inflation of body to crack cuticle

juvenile hormone:

  • reduces with each moult
  • determines form of next stage: zero JH produces adult

application:
pre adult fleas in larval stage are fed through he faeces of the parents. if excess JH is released, it means the larvae will not form into pupae and thus be prevented from developing into fleas
- the pupae is too large to survive
- cannot go into moulting stage

42
Q

describe biological controls for organisms other than predators and parasites

A

the basic strategy refers to investigation of the biology of the pest, this refers to local research, life cycle, weak points e.t.c.

some examples of methods are:

  • drain pools and swamps for mosquito larvae in ponds
  • monolayer dispersants on water surfaces also for mosquito larvae
  • traps baited with food smell and this is used on the tsetse fly with ox blood
  • traps and tubes with female pheromones for the cabbage moths
43
Q

list biological controls for predators

A
  1. predatory insects-some prey on mosquitoes
  2. spiders and predatory mites can be used for sustainable agriculture
  3. fish: has many species such as instant fish, these can lay eggs that can survive when water is drained and then when there is finally water, can feed on the mosquitoes
  4. parasitoid wasps can hatch eggs in other organisms and use it as a feeding for the eggs
44
Q

describe the ideal predatorily control

A
  • initially, the predator increases rapidly whilst the number of pests are high, therefore as predators increase, pests decrease
  • then the predators drop rapidly, but not to extent of elimination, or else, would have to introduce again when pest comes back
  • this is all to get a stable interaction between pest and predator when there are low pest levels
45
Q

list desirable features of predators

A
  1. fairly specific as to the prey it eats
    - same habitats as pest
    - rapid rate of increase
    - disperse easily
    - population size not kept low by environment
    - survives when pest at low levels and thus there is a STABLE INTERACTION
    - easily cultured
46
Q

list examples of biological control of parasites

A

bacteria: Bacteria thuringensis (BT) kills manu insects
virus: nuclear polyhedrons virus in insects
Fungi: Tolypocladium may control mosquitoes, coelomomycos kills the mosquito larvae
Nematodes: kill infected insects and can carry bacteria too

47
Q

describe parasites of parasites

A

wolbachia bacterium manipulates the filarial worm to reproduce rapidly causing elephantiasis, but a virus: bacteriophage attacks Wolbachia

bacteriophage>wolbachia>filarial worm>elephantiasis

48
Q

describe wolbachia

A
  • bacteria that live inside insect cells
  • cause incompatible matings and this helps them spread into insect populations
    + they get into the immature spermatids and the eggs of the insects, and if sperm from infected insects fertilises uninfected eggs the offspring die, but infected eggs produce offspring
  • this means if you add enough infected, you take over pop.
  • they can also suppress virus transmission
49
Q

describe the two methods of genetic control

A

eg, sterile male screw worm fly had a present barrier and proposed barrier. it was effective. because the sterile males could mate with the females which could only mate once

1: Introduce a genetic load(of bad genes) and spread these bad genes through the population: (do this by)
- use recombinant DNA technology by introducing bad alleles
- delayed sterility where it occurs in later generations
- conditional lethal genes eg. vulnerability to cold
- more sexually active males
- meiotic drive whereby one pair of a chromosome goes into all the gametes ensuring bad genes get into offspring

2:reduce or replace posts:
- reduce the pest by introducing an incompatible competing strain such as wolbachia: works on the basis of compound chromosomes and there associated mating outcomes
+a strain that produces dead offspring if it reproduces with wild types
+ but it can reproduce with itself, and you can select the alleles it has
- replace vectors with incompatible strains that don’t carry the disease
- replace pest by an easily controlled strain

Genes and Environment (12 decks)

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