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genetics > 8a&b - Meiosis & Genetics > Flashcards

8a&b - Meiosis & Genetics Flashcards

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Biology 101 flashcards
1
Q

behaviour of chromosomes during meiosis can explain Mendel’s hereditary “factors”

A
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2
Q

Mitosis is a nuclear division that produces two genetically identical daughter cells

A
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3
Q

Meiosis is a nuclear division that produces gametes by reducing the number of chromosomes

A
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4
Q

Demonstrate an appreciation for why understanding meiosis is so critical to understanding genetics

A
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5
Q

Work problems that illustrate the importance of meiosis to the laws of Segregation and Independent Assortment

A
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6
Q

how do we know Mendel’s factors are associated with chromosomes?

A
  • in 1800s, cytologists saw chromosomes & realised they behaved just like Mendel’s factors
  • they were able to show that genes are found on chromosomes
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7
Q

mitosis in 4 stages

A
  1. PROPHASE -> chromosomes start to condense, as they become visible they appear doubled
    -> nuclear envelope begins to break down
  2. METAPHASE -> nuclear spindle forms
    -> chromosomes line up at equator
  3. ANAPHASE -> poles move apart
    -> centromeres split & chromatids separate (1 of each pair moving to pole)
  4. TELOPHASE -> nuclear membrane reforms & chromosomes decondense
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8
Q

At fertilisation, 2 gametes fuse to form new individual, but number of chromosomes stays constant from generation to generation

How?

A

Formation of gametes involves a special type of nuclear division that halves chromosome number

2 division events:

  • Meiosis I = reductive division
  • Meiosis II = separation of sister chromatids
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9
Q

If a geneticist were to closely examine make-up of single autosomal chromosome from 1 of your cells, that chromosome would be found to be, What?????

asking about RECOMBINATION

A

mosaic of genes derived from 2 of your grandparents (either maternal / paternal)

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10
Q

changes in chromosome no.

8b

A
  1. organisms with multiples of basic chromosome set referred to as ‘euploid’
  2. individs whose chromosome no. differs by small no. of chromosomes is referred to as
    ‘aneuploid’
  3. how do cells end up with too many / too few chromosomes?
  4. why does having extra chromosomes affect the phenotype so drastically?
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11
Q

euploid

A

organisms with multiples of basic chromosome set

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12
Q

aneuploid

A

individs whose chromosome no. differs by small no. of chromosomes

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13
Q

changes in chromosome structure

A
  1. chromosome can have missing pieces: deletions
  2. chromosomes can have extra pieces: duplications
  3. chromosomes can have mixed-up pieces: inversions
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14
Q

Chinese & Indian muntjac are closely related sp

they have diff no. of chromosomes (euploid) BUT same no. of genes

how / why does this occur?

A

-> eukaryotes are haploid / diploid, with 1 or 2 complete sets of chromosomes, respectively

-> organisms that have more / fewer than normal no. of chromosomes are aberrant euploids:

  • polyploids have >2 chromosome sets
  • polyploids can be triploid, tetraploid, pentaploid & so forth
  • individ of a typically diploid sp that has only 1 set of chromosomes is called a monoploid (rather than haploid which is the normal condition for some sp)
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15
Q

polyploid

A

have >2 chromosome sets

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16
Q

monoploid

A

individ of typically diploid sp with only 1 set of chromosomes

^diff than haploid which is normal condition for some sp

17
Q

aberrant euploids

A

organisms with more / fewer than normal no. of chromosomes

18
Q

Does polyploidy / monoploidy always result in abnormal development?

A

no!!!!

  • male bees, wasps, & ants are monoploid developing from unfertilised eggs
  • polyploidy v common in plants, less common in animals…
  • BUT does occur in eg. group of Australian frogs & tetraploid Pacific oyster
19
Q

how do cells end up with too many / too few chromosomes?

A
  • cause of most aneuploidy is non-disjunction during meiosis / mitosis
  • for our case, mostly during formation of gametes
20
Q

examples of extra chromosomes affecting phenotype drastically

A

eg.s of human genetic diseases caused by changes in chromosome no:

  • any monosomics for autosomes in humans die in utero, but monosomy for X (in 75-80% of cases it is caused by a missing X chromosome in the father’ s sperm) causes Turner syndrome
  • many trisomys are lethal, however there are a no. of eg.s of viable trisomics, including trisomy 21 (in 90% of cases it is caused by non-disjunction in the mother’s egg) causes Down syndrome
  • Klinefelter syndrome results from XXY karyotype (extra chromosome comes from both mother & father in this case)
21
Q

why are aneuploids so much more abnormal than polyploids?

A
22
Q

why does aneuploidy for each chromosome have its own characteristic phenotypic effects?

A
23
Q

why are monosomics typically more severe than the corresponding trisomics?

A
  • any monosomics for autosomes in humans die in utero…
  • so monosomics only happen in X chromosome…
  • causing things like Turner Syndrome
24
Q

gene balance

A
  • genes have evolved to function in diploid genetic background …
  • & disrupting that background disrupts their function
25
Q

Haplo-abnormal genes

A

genes that cannot function properly as single copy

26
Q

Triplo-abnormal genes

A

abnormalities caused by 3 copies

27
Q

Why does having extra chromosomes affect the phenotype so drastically?

A

gene balance - genes have evolved to function in diploid genetic background & disrupting background disrupts their function

  • haplo-abnormal genes
  • triplo-abnormal genes
  • expression of deleterious alleles on monosomic autosomes (in absence of wild type counterpart)
  • having only 1 gene copy (monosomic) is worse than having three (trisomic)
28
Q

chromosomes can have missing pieces: deletions

big changes in chromosome structure

A
  • deletion: loss of part of 1 chromosome arm
  • deletions can be small, only covering part of 1 gene
  • deletions can be large, with chromosomes missing pieces large enough to be visualised on a karyotype
29
Q

Cri-du-chat (cat’ s cry) syndrome

large deletion eg.

A
  • deletion of end of short (p) arm of chromosome 5 (5p- OR 5p minus)
  • signs & symptoms related to loss of multiple genes in this region
  • larger deletions => more severe intellectual disability & developmental delays
  • specific regions associated with specific problems:
    -> 5p15.3= cat-like cry,
    -> 5p15.2=intellectual disability/microcephaly
30
Q

Williams syndrome

small deletion eg.

A

-> deletion of 1 out of 2 copies of elastin gene

-> smaller deletions visualised using ‘FISH’

-> more than 25 genes deleted on chromosome 7, for example…

  • ELN (elastin) gene= connective tissue abnormalities & CVD
  • CLIP2, GTF21, GTF2IRD1, LIMK1 =problems with visual spatial tasks
  • NCF1 (Neutrophil Cytosolic Factor 1)= related to risk of developing hypertension if NOT deleted (part of NADPH oxidase which increases reactive O₂ sp & blood vessel changes)

-> most not inherited -> random events during production of eggs / sperm (no history in family)

31
Q

chromosomes can have extra pieces: duplications

A
  • duplications play import role in evolution of genome (e.g. P450s like Cyp6g1 &
    Суp6g2)
  • duplication allows for divergence -> so Cyp6g1 can go become insecticide resistantance gene & Cyp6g2 can perform more basal function (eg. metabolising hormones)
32
Q

chromosomes can have mixed-up pieces: inversions & translocations

A
  • to create an inversion, segment of chromosome is cut out, flipped & reinserted into chromosome in opp. orientation
  • inversions are “balanced” rearrangements - don’t involve gain / loss of genetic material
  • BUT during meiosis, inversions can => duplications & deletions
  • important in locking unique combinations of alleles/genes together

-> “locking” = no recombination

33
Q

eg. of adaptive inversion

A
  • P locus of Heliconius numata & supergene for mimicry (special topic on butterflies)
  • diff inversions lock diff gene combinations = diff colour morphs
34
Q

chromosomes can have mixed-up pieces: inversions & translocations

A
  • translocation: rearrangement involving part of 1 chromosome that has broken off & reattached to diff chromosome
  • Reciprocal translocations
  • Robertsonian translocations
35
Q

reciprocal translocations

A
  • exchange between nonhomologous chromosomes
  • 1 / 500 newborns
  • usually harmless…
  • BUT carriers of balanced translocations have risk of creating gametes with unbalanced translocations (miscarriage / abnormality)
36
Q

Robertsonian translocations

A
  • joining of 2 acrocentric chromosomes (centromere not central) at centromeres with loss of their short arms
  • humans have only 45 chromosomes in each cell
  • appear normal…
  • BUT their children may be normal & carry fusion chromosome…
  • OR inherit missing / extra long arm of acrocentric chromosome
  • genetic testing and counseling

genetics (7 decks)

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