d2.1 cell and nuclear division Flashcards
mitosis
process of cell division where one cell divides into two genetically identical daughter cells
function of mitosis [2]
- for growth and repair of tissues
- to control cell size
unequal cytokinesis + examples [2]
uneven division of cytoplasm during cell division
- exceptions
———–
1. oogenesis in humans
2. budding in yeast
outline of prophase
- chromosome become condensed and visible by supercoiling
- nuclear membrane breaks down
- centriole starts forming spindle microtubules
outline of metaphase
- centrioles form spindle microtubules that attach to the centromere of the chromosome
- chromosomes line up at the equator
outline of anaphase
- centromere divides
- sister chromatid separates + move to opposite poles
- spindle fiber contract
outline of telophase
- spindle fibre breaks down
- nuclear membrane reform
- chromosome uncoiled and no longer visible
difference between mitosis and cytokinesis
mitosis is the division of the nucleus
cytokinesis is the division of the cytoplasm- cells are formed
cytokinesis in animal cells
- 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
cytokinesis in plant cells
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.
function of meiosis
production of haploid gametes
homologous chromosome
chromosomes that has the same gene loci but not necessarily same allele
why meiosis is a reduction division
results in production of nuclei where the number of chromosomes is halved from the parent diploid nucleus
- from diploid (2n) to haploid (n)
result of crossing over
formation of new combination of alleles which in turn result in variation in gametes
how random orientation in metaphase I leads to further genetic variation + number of possible orientations in human cells
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
why random orientation in metaphase II is less important to genetic variation than
random orientation in metaphase I
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
interphase
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
cell cycle
all stages in the life cycle of a cell
cytokinesis
division of the cytoplasm and hence forming two separate cells
- both daughter cells must receive at least one mitochondrion
apoptosis
programmed cell death, where the death of cells which occurs as a normal and controlled part of an organism’s growth or development
necrosis
death of most or all of the cells in an organ or tissue due to disease, injury or failure of the blood supply
diploid
cell that have two complete sets of chromosomes, one from each parent
haploid
cell that have a single set of unpaired chromosomes
G1 phase [3]
- increase the volume of cytoplasm
- organelles produced
- proteins synthesised
S phase
DNA replicated
G2 phase [3]
double checks G1 processes
- increase the volume of cytoplasm
- organelles produced
- proteins synthesised
metabolic reactions that occur during interphase [4]
- metabolic reactions- necessary for the life of the cell
eg. respiration to produce ATP - protein synthesis- proteins and enzymes are necessary to allow cell growth
- organelles numbers are increased- support the enlarged cell
- DNA is replicated- ensure a second copy is available to enable mitosis
cyclin
family of proteins that control the progression of cells through the cell cycle
how cyclins control the progression of a cell through the cell cycle
each different cyclin reaches a certain concentration (threshold level) -> triggers next stage of cell cycle
cyclin A function
activates DNA replication inside the nucleus in S phase
cyclin B function
promotes the assembly of the mitotic spindle and other tasks in the cytoplasm to prepare for mitosis
cyclin D function
triggers cells to move from G0 to G1 and from G1 to S phase
cyclin E function
prepares the cell for DNA replication in S phase
cyclin conc graph
pic
tumour
abnormal growth of tissue that develop at any stage of life in any part of the body
metastasis
movement of cells from a primary tumour to set up secondary tumours in other parts of the body, through the bloodstream or lymphatic stream
primary tumour
malignant tumour growing at the site where abnormal growth first occurred
how primary cells develop into secondary cells
- detach from the primary tumour
- some gain the ability to penetrate the walls of lymph or blood vessels -> can circulate the body
- circulating cancerous cells invade tissues at different locations and develop by uncontrolled cell division -> secondary tumours
oncogenes
few genes that can become cancerous after mutating
- mutated from pronto-oncogenes
- causes rapid uncontrolled division
role of oncogenes in normal, healthy cells
control cell cycle and cell division
why a mutation in oncogenes can result in cancer
mutation in a oncogene -> malfunction in the control of the cell cycle -> uncontrolled cell division -> tumour formation
mutagens
chemicals that cause mutations
example of non-chemical mutagens
exposure to high energy radiation
factors that increase the probability of tumour development in humans [3]
- exposure to mutagens
- vast number of cells in the body- higher change
- longer the life span, greater chance of mutation
in all living organisms, a parent cell…
divides to produce two daughter cells
why is nuclear division needed before cell division
avoid production of anucleate cells
mitosis maintains… [2]
- chromosome number
- genome of cells
result of meiosis
- halves the chromosome number
- generates genetic diversity
role of histones
condenses the DNA by supercoiling
use of microtubules and microtubule motors
move chromosomes
result of error in meiosis
down syndrome
how does meiosis generate genetic diversity [2]
- random orientation of bivalents
- crossing over
chromatin made up of
dna and histone
- supercoiled into nucleosome
when does chromatin condense
prophase
nucleosome made up of + draw
DNA and 8 histone proteins
- notes
genotype
combination of alleles that determine the phenotype
phenotype
observable trait
loci
location of gene in a chromosome
centromere
centre of chromatid
- use it to count
genes
length of DNA that contains genetic information to synthesise a polypeptide
mechanism of cyclin action
- Activate enzymes (cyclin dependent kinases) → bind phosphate to other proteins (complex phosphorylates), (diff type of cyclin binds phosphate to diff protein) → trigger specific event
- 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
hayflick limit
number of possible cell division and depends on the length of chromosomal telomeres
telomere
regions of repetitive DNA located at each end of a chromatid
function of telomere
prevent chromosomal deterioration
why doesnt the telomere become super long
extreme ends of telomeres cannot be copied during DNA replication- get shorter
what only happens in meiosis [2]
- crossing over
- homologous chromosomes move to the equator in pairs
what turns normal cells into tumour cells
- through gene mutations
1. inheritance
2. random changes during transcription
3. mutagens
4. gamma rays
pronto-oncogenes
genes that cause normal division
tumour-suppressor genes
genes that inhibit division
- if mutated, nothing to control cell division
recombinant
swapped the alleles between non-sister chromatids
synapsis
- may or may not happen
- homologous chromosomes pair up to form a bivalent
- further away from nucleus- more likely
chiasma formation
- neighbouring non-sister chromatids cut at the same point
- crosses/overlap
- genetic information may swap
if crossing over occurs what happens to the sister chromatids
no longer identical
when can crossing over occur
prophase I
pairs of sister chromatids that are visible during meiosis, what are they a result of
result from the replication of DNA before meiosis
