d2.1 cell and nuclear division Flashcards

1
Q

mitosis

A

process of cell division where one cell divides into two genetically identical daughter cells

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2
Q

function of mitosis [2]

A
  1. for growth and repair of tissues
  2. to control cell size
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3
Q

unequal cytokinesis + examples [2]

A

uneven division of cytoplasm during cell division
- exceptions
———–
1. oogenesis in humans
2. budding in yeast

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4
Q

outline of prophase

A
  • chromosome become condensed and visible by supercoiling
  • nuclear membrane breaks down
  • centriole starts forming spindle microtubules
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5
Q

outline of metaphase

A
  • centrioles form spindle microtubules that attach to the centromere of the chromosome
  • chromosomes line up at the equator
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6
Q

outline of anaphase

A
  • centromere divides
  • sister chromatid separates + move to opposite poles
  • spindle fiber contract
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7
Q

outline of telophase

A
  • spindle fibre breaks down
  • nuclear membrane reform
  • chromosome uncoiled and no longer visible
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8
Q

difference between mitosis and cytokinesis

A

mitosis is the division of the nucleus
cytokinesis is the division of the cytoplasm- cells are formed

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9
Q

cytokinesis in animal cells

A
  • ring of contractile actin and myosin proteins pinches a cell membrane together to split the cytoplasm
  • inward pull on the plasma membrane produces the cleavage furrow
  • when the cleavage furrow reaches the centre of the cells, it is pinched apart to form two daughter cells
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10
Q

cytokinesis in plant cells

A

telophase: membrane-enclosed vesicles derived from the golgi apparatus migrate to the centre of the cell

vesicles assemble section of membrane and cell wall to achieve splitting

  • Vesicles fuse to form tubular
    structures.
  • The tubular structures merge to form
    two layers of plasma membrane (cell plate)
  • cell plate develops until it connects with the existing cell’s plasma membrane.
  • Vesicles deposit pectins and other substances in the lumen between the daughter cells to form the middle lamella using exocytosis
  • Both daughter cell secrete cellulose
    to form their new adjoining cell walls.
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11
Q

function of meiosis

A

production of haploid gametes

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12
Q

homologous chromosome

A

chromosomes that has the same gene loci but not necessarily same allele

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13
Q

why meiosis is a reduction division

A

results in production of nuclei where the number of chromosomes is halved from the parent diploid nucleus
- from diploid (2n) to haploid (n)

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14
Q

result of crossing over

A

formation of new combination of alleles which in turn result in variation in gametes

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15
Q

how random orientation in metaphase I leads to further genetic variation + number of possible orientations in human cells

A

orientation of one bivalent does not influence the orientation of any of the others and is random
- promotes genetic variation among genes that are on different
chromosome types
- 2^23

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16
Q

why random orientation in metaphase II is less important to genetic variation than
random orientation in metaphase I

A

metaphase ii- sister chromatids separate which are not as dramatically different as homologous
chromosomes are
- differences in sister chromatids only at places where crossing over has
taken place
- random orientation of sister chromatids contributes not as much as than random orientation of homologous chromosomes that happens in metaphase i to variation
- Homologous chromosomes can be significantly different from each other with different types of alleles

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17
Q

interphase

A

very active phase of the cell cycle with many processes occurring in the nucleus and cytoplasm
- consists of the parts of the cell cycle that dont involve cell division

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18
Q

cell cycle

A

all stages in the life cycle of a cell

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19
Q

cytokinesis

A

division of the cytoplasm and hence forming two separate cells
- both daughter cells must receive at least one mitochondrion

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20
Q

apoptosis

A

programmed cell death, where the death of cells which occurs as a normal and controlled part of an organism’s growth or development

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21
Q

necrosis

A

death of most or all of the cells in an organ or tissue due to disease, injury or failure of the blood supply

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22
Q

diploid

A

cell that have two complete sets of chromosomes, one from each parent

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23
Q

haploid

A

cell that have a single set of unpaired chromosomes

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24
Q

G1 phase [3]

A
  • increase the volume of cytoplasm
  • organelles produced
  • proteins synthesised
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25
Q

S phase

A

DNA replicated

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26
Q

G2 phase [3]

A

double checks G1 processes
- increase the volume of cytoplasm
- organelles produced
- proteins synthesised

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27
Q

metabolic reactions that occur during interphase [4]

A
  1. metabolic reactions- necessary for the life of the cell
    eg. respiration to produce ATP
  2. protein synthesis- proteins and enzymes are necessary to allow cell growth
  3. organelles numbers are increased- support the enlarged cell
  4. DNA is replicated- ensure a second copy is available to enable mitosis
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28
Q

cyclin

A

family of proteins that control the progression of cells through the cell cycle

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29
Q

how cyclins control the progression of a cell through the cell cycle

A

each different cyclin reaches a certain concentration (threshold level) -> triggers next stage of cell cycle

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30
Q

cyclin A function

A

activates DNA replication inside the nucleus in S phase

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31
Q

cyclin B function

A

promotes the assembly of the mitotic spindle and other tasks in the cytoplasm to prepare for mitosis

32
Q

cyclin D function

A

triggers cells to move from G0 to G1 and from G1 to S phase

33
Q

cyclin E function

A

prepares the cell for DNA replication in S phase

34
Q

cyclin conc graph

A

pic

35
Q

tumour

A

abnormal growth of tissue that develop at any stage of life in any part of the body

36
Q

metastasis

A

movement of cells from a primary tumour to set up secondary tumours in other parts of the body, through the bloodstream or lymphatic stream

37
Q

primary tumour

A

malignant tumour growing at the site where abnormal growth first occurred

38
Q

how primary cells develop into secondary cells

A
  1. detach from the primary tumour
  2. some gain the ability to penetrate the walls of lymph or blood vessels -> can circulate the body
  3. circulating cancerous cells invade tissues at different locations and develop by uncontrolled cell division -> secondary tumours
39
Q

oncogenes

A

few genes that can become cancerous after mutating
- mutated from pronto-oncogenes
- causes rapid uncontrolled division

40
Q

role of oncogenes in normal, healthy cells

A

control cell cycle and cell division

41
Q

why a mutation in oncogenes can result in cancer

A

mutation in a oncogene -> malfunction in the control of the cell cycle -> uncontrolled cell division -> tumour formation

42
Q

mutagens

A

chemicals that cause mutations

43
Q

example of non-chemical mutagens

A

exposure to high energy radiation

44
Q

factors that increase the probability of tumour development in humans [3]

A
  1. exposure to mutagens
  2. vast number of cells in the body- higher change
  3. longer the life span, greater chance of mutation
45
Q

in all living organisms, a parent cell…

A

divides to produce two daughter cells

46
Q

why is nuclear division needed before cell division

A

avoid production of anucleate cells

47
Q

mitosis maintains… [2]

A
  1. chromosome number
  2. genome of cells
48
Q

result of meiosis

A
  • halves the chromosome number
  • generates genetic diversity
49
Q

role of histones

A

condenses the DNA by supercoiling

50
Q

use of microtubules and microtubule motors

A

move chromosomes

51
Q

result of error in meiosis

A

down syndrome

52
Q

how does meiosis generate genetic diversity [2]

A
  1. random orientation of bivalents
  2. crossing over
53
Q

chromatin made up of

A

dna and histone
- supercoiled into nucleosome

54
Q

when does chromatin condense

A

prophase

55
Q

nucleosome made up of + draw

A

DNA and 8 histone proteins
- notes

56
Q

genotype

A

combination of alleles that determine the phenotype

57
Q

phenotype

A

observable trait

58
Q

loci

A

location of gene in a chromosome

59
Q

centromere

A

centre of chromatid
- use it to count

60
Q

genes

A

length of DNA that contains genetic information to synthesise a polypeptide

61
Q

mechanism of cyclin action

A
  1. Activate enzymes (cyclin dependent kinases) → bind phosphate to other proteins (complex phosphorylates), (diff type of cyclin binds phosphate to diff protein) → trigger specific event
  2. At the same time, reaches the threshold level
    - CDK releases phosphate → cyclin breaks down → CDK inactive
    - Ensures key processes (DNA replication/protein synthesis) to occur at correct time
62
Q

hayflick limit

A

number of possible cell division and depends on the length of chromosomal telomeres

63
Q

telomere

A

regions of repetitive DNA located at each end of a chromatid

64
Q

function of telomere

A

prevent chromosomal deterioration

65
Q

why doesnt the telomere become super long

A

extreme ends of telomeres cannot be copied during DNA replication- get shorter

66
Q

what only happens in meiosis [2]

A
  • crossing over
  • homologous chromosomes move to the equator in pairs
67
Q

what turns normal cells into tumour cells

A
  • through gene mutations
    1. inheritance
    2. random changes during transcription
    3. mutagens
    4. gamma rays
68
Q

pronto-oncogenes

A

genes that cause normal division

69
Q

tumour-suppressor genes

A

genes that inhibit division
- if mutated, nothing to control cell division

70
Q

recombinant

A

swapped the alleles between non-sister chromatids

71
Q

synapsis

A
  • may or may not happen
  • homologous chromosomes pair up to form a bivalent
  • further away from nucleus- more likely
72
Q

chiasma formation

A
  • neighbouring non-sister chromatids cut at the same point
  • crosses/overlap
  • genetic information may swap
73
Q

if crossing over occurs what happens to the sister chromatids

A

no longer identical

74
Q

when can crossing over occur

A

prophase I

75
Q

pairs of sister chromatids that are visible during meiosis, what are they a result of

A

result from the replication of DNA before meiosis