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Genetics > Lecture 9 > Flashcards

Lecture 9 Flashcards

1
Q

What is a gene interaction?

A

-when two or more genes influence the same phenotypic trait -two genes or more interacting to determine one trait -genes interacting and dependant upon each other to produce a particular phenotype

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2
Q

Give an example of gene interaction.

A

e.g.: coat colour BB;DD x bb;dd still get 9:3:3:1 ratio but only one phenotypic trait D- densely aggregated pigment d-more dilute pigment so paler colours DD dd- dense/ dilute locus controls the distribution of coloured pigment granules= it is the modifier gene

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3
Q

What are the biochemical pathways in gene interaction? (coat colour Bb and coat Dd=dense/diluted)

A
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4
Q

What is epistasis?

A

an allele at one gene locus masks the phenotypic expression of the alleles of another gene locus

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5
Q

Does epistasis change the phenotypic ratio?

A

-alters the phenotypic ratios since we can’t get some phenotypes due to the presence of aa (in case of the agouti) then the pathway to B black is masked so even if the animal has it it won’t be expressed
aa is epistatic to B
ratio: 9:3:4 (agouti, black, albino)

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6
Q

What is recessive epistasis?

A

: when have to have aa to mask the otehr gene, ratio 9:3:4

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7
Q

What is dominant epistasis?

A

even just one dominant allele will lead to masking of the other gene, ratio 12:3:1

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8
Q

What does it mean when phenotypic ratio adds up to 16?

A

working with two genes!

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9
Q

How many blood groups are there?

A

-over 400 bllod group antigens decsribed in humans

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10
Q

Which two systems of blood groups are important for blood transfusion?

A

ABO and Rhesus

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11
Q

Do blood groups occur in other animals?

A

-yes (canine blood bank)

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12
Q

What is an antigen?

A

antibody generator so bacteria, virus, pollen, any compound that will result in antibody generation

flu=antigen our body produces antibody

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13
Q

What is an antibody?

A

= the molecule that is produced in response to the antigen

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14
Q

Where are A and B antigens located?

A
  • on the surface of a blood cell (they are glycoproteins= sugar with a protein attached)
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15
Q

What is the dominance relationship between IA IB and IO?

A

IA and IB are codominant; IA and IB are dominant to IO

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16
Q

How is the blood type determined in development by genes? (picture)

A

If have only IO than H structure stays as it is if IA then add N-acetylgalactosamine(sugar) to H and IB add galactose to H structure

17
Q

Does everyone have the H structure?

A

yes,not all H is converted

18
Q

What are the possible genotypes for blood groups A, B and O and AB? And the antigenon the surface of the cell?

A
19
Q

What antibody and antigen do all the ABO blood groups have?

A
20
Q

How do we determine a person’s blood type?

A

Take blood sample and add antisera containing known antibodies and wait to see what will agglutinate.

Type A, AB- agglutination with antiA (containing antibody A)
Type B, AB- agglutination with antiB (containing antibody B)
Type O no agglutination anti A or B (containing both antibody A and B)

21
Q

What happens when we have a matching antigen and antibody in blood?

A

Results in agglutination then death! Has to be treated within 20mins.

blood cells bound together, can’t transfer O2=death

22
Q

Which blood group is the universal donor and why?

A

Type O, becaus eit doesn’t have any antigens on the blood cells so won’t agglutinate with any other blood

23
Q

Which blood group is the niversal recipent and why?

A

Type AB, because it doesn’t have any antibodies.

24
Q

Why can antigen A and antibody B coexist in a person?

A

can co-exist together, don’t attach to each other, no match

25
Q

What is the key factor in blood transfusions?

A
  • key factor is the antigen on the surface of the red blood cells(rbcs) of the donor
  • if the rbcs of the donor have the antigen for which the recipient has the antibody- agglutination will result
  • reverse doesn’t cause problems because the antibody from the donor gets diluted and it doesn’t agglutinate
  • parents store chord blood for later transfusions and treatment e.g. leukemia
26
Q

What blood can type A, B, AB and O get?

A

Type A can get blood from A,O
Type B can get blood from B,O
Type AB can get blood from A, B, O, AB
Type O can get blood from O

27
Q

When does the Bombay genotype arise?

A

Have parents eg. Type A man and O mother, have B child

  • to get the H structure, have to have HH or Hh alleles if homozygous recessive hh then the person doesn’t develop the the antigens. So the woman had AB but was hh so didn’t get the precursor for IA or IB and tested as type O, her child got the B from her
  • recessive epistasis hh masks B
  • FUT 1 gene= bombay gene
28
Q

How common is the absence of antigen H?

A
  • Bombay phenotype
  • 1/8000 in Taiwan
  • 1/10 000 in India
  • 1/1 000 000 in Europe
29
Q

What blood can Bombay phenotype person receive?

A

People with Bombay phenotype produce antibody H, A and B so can only receive blood from another Bombay phenotype

30
Q

How do you distinguish between Bombay and true type O?

A

-use antibody H, Type O would agglutinate because they have antigen H but Bombay wouldn’t as it doesn’t have any antigens

31
Q

Describe the MN blood system?

A
  • another system of blood groups
  • 1 gene locus chromosome 4
  • 2 alleles LM and LN –codominant
  • not relevant for blood transfusion as no antibodies for these in the blood plasma

LMLM phenotype M antigen M
LMLN phenotype MN antigens M and N
LNLN phenotype N antigen N

32
Q

Describe the Rhesus system?

A

-blood group system
-chromosome 1
-2 alleles D and d, complete dominance
-3 genotypes DD,Dd,dd
-2 phenotypes: Rhesus +ve (DD, Dd) approx 85% Australians =have the antigen D
Rhesus –ve (dd) =allele that does nothing, no antigen D

33
Q

What are the possible issues with Rhesus in transfusions?

A

If –ve receives +ve blood
= the first transfusion ok, but the incoming antigen D triggers production of the antibody and sentisizes the –ve person
=second transfusion! Danger of death!
-in an emergency male can get +ve blood (if it’s the first time)
-never given to a female of reproductive age= pregnancy then at risk

34
Q

What is the Haemolytic disease of the newborn (erythroblastosis fetalis)?

A

-arises when Rh-ve mother (dd) carrying Rh+ve (Dd)
- if parents ddxDD or ddxDd
=Dd all at risk =1/2 Dd-at risk, ½ dd no risk

  • during pregnancy and birth fetal rbcs may enter mother’s body= antibodies produced
  • first pregnancy usually fine (first exposure to D antigen in the mother)
  • but then D antibodies from the mother cross the placenta and agglutinate rbcs of the fetus= death
35
Q

How is Haemolytic disease of the newborn prevented/treated?

A

: RhoGAM Rho(D) Immune Globin given to Rh.ve woman shortly after delivery, miscarriage or abortion. Also given to pregnant women after amniocentesis, any bleeding episodes plus seventh month of pregnancy.

  • injection at 28 weeks of pregnancy and after birth
  • the Rho(D) Immune globulin contains antibodies to the Rh D antigen-these antibodies destroy any red blood cells from the baby that have entered mother’s blood
  • D antibody D antigen=they do agglutinate and die but it won’t kill the mother because she will have only few of those cells in her blood= won’t affect oxygen carrying capacity!
36
Q

Can there be an issue in pregnancy with ABO groups?

A

ABO incompatibility:

  • blood type where the baby is either A or B or AB bood type and mother type O
  • blood from fetus in contact with maternal blood means antigen is in contact with antibody
  • less than 1% of type O mothers
  • the babies born jaundiced (yellowy) treated with UV light and then OK

Genetics (40 decks)

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