Mitosis - the only way to get new genetically identical cells
somatic cells - normal body cells
meiosis - produces genetically different daughter cells galled gametes responsible for reproduction
chromosome - single long DNA strand wrapped around histones and containing genes
one chromosome has many genes, which code for products
unreplicated chromosome → replicated chromosome → condensed replicated chromosome
even when chromosomes copy, if they are attached to each other they are one chromosome; this is known as sister chromatids, which remain joined at the centromere until they are separated during cell division.
m-phase: mitosis or meiosis
interphase: gap 1, s-phase, gap 2
these contain checkpoints to ensure cell properly divides
chromosome NEVER changes during mitosis
prophase - chromosomes condense, spindles form
spindles are made of microtubules and are able to move chromosomes and pull chromatids apart
centrioles move to opposite ends of the cell
prometaphase
nuclear envelope breaks so microtubules can attach to chromosomes at kinetochores
kinetochores are structures on the centromere of sister chromatids
they are proteins providing a site of connection
metaphase - central alignment of chromosomes
spindle fibers move chromosomes to metaphase plate and are anchored to cell membrane
anaphase
microtubules shorten and pull sister chromatids apart, ensuring each daughter cell receives the same number of chromosomes
because sister chromosomes are not attached, they are now called chromosomes
telophase
reformes nuclear envelope and chromosomes recondense in each daughter cell
each daughter cell now has unreplicated chromosomes
cytokinesis - splitting of cytoplasm
plants build a new cell wall with their cell plates
animals just split membrane in half
this process happens with actin and myosin proteins, creating cleavage furrows
prokaryotic division - binary fission
prokaryotes do not have nuclei or spindle fibers
replicate circular chromosomes and undergo the same process
chromosomes
homologs - chromosomes of same size and shape with same genes in same place
sister chromatids - identical PART of a chromosome
non-sister chromatid - one chromatid is on one homolog and a separate chromatid is on a different homolog
meiosis - goal of halving chromosomes and producing gametes
increases genetic diversity
chromosome number is restored during fertilization
all organisms have a specific number of chromosomes unique to them
x and y are sex chromosomes
chromosome pairs that do not determine sex are called autosomes
homologous chromosomes: NOT identical
bivalence: paired, replicated homologs attached during prophase I
ploidy
number of chromosome pairs
n is the number of unique chromosomes in a cell
haploid: meaning single form, denoted by n, one distinct type of chromosome
diploid: meaning double, denoted by 2n, one paternal and one maternal chromosome
polyploidy: 3 or more of each unique chromosome
ploidy changes throughout an organisms life cycle
haploid gametes combine to form diploid zygotes
then diploid zygotes undergo mitosis and develop into diploid adults
priori to meiosis
chromosomes always replicate in s-phase
checkpoints remain the same and now pairing matters
two complete cell divisions
meiosis 1: homologous chromosomes separate
meiosis 2: sister chromatids separate
meiosis 1 - promoting genetic variation via crossing over, creating new allele combinations
prophase 1 - undergoes synapsis, create chiasmata, and complete crossing ober
homologs come close together and become bivalent during synapsis
chiasmata - non-sister chromatids join and prepare to cross over
crossing over - non-sister chromatids exchange genetic information at genes / alleles
metaphase 1 - homologs line up at the metaphase plate
anaphase 1 - homologous pairs separate into individual replicated chromosomes
crossing over - genetic recombination
independent assortment - the way homologs align at metaphase plate
fertilization - union of two random gametes
outcrossing and self pollination
Nondisjunction - either homologs or sister chromatids fail to separate
aneuploidy - cells have an abnormal amount of chromosomes
if nondisjunction occurs in meiosis 1, two n+1 cells and two n-1 cells are produced
karyotype: visualization of all chromosomes to find aneuploidy
trisomy-21: three chromosomes are at chromosome 21, cause of down syndrome
cell cycle regulation
checkpoints cause cell to stay in that phase until it’s ready for division
g1: is the cell large enough, does it have enough nutrients, are social signals present and is the DNA undamaged?
g0: mature / unfixable cells never pass through this checkpoint
g2: have the chromosomes been successfully replicated and is the DNA undamaged?
m-phase
checkpoint between prometaphase and metaphase ensuring spindle fibers properly attached and the chromosomes properly separate
proteins
cyclins: only produced when needed in a specific part of the phase
at G1, G1 to S phase, S phase and M phase
work with cyclin-dependent kinases (cdks)
only work when paired with cyclin
activate protein by removing phosphate from ATP and donate to a specific protein
MPF: m-phase promoting factor
cyclin and cdk pair in the cytoplasm telling the cell it’s ready for mitosis
cyclin is produced in g1 and peaks during m-phase
binds to cdk and activates it, cycling concentration goes down until the cell is ready for another cycle
regulation of MPFs
interphase
cyclin concentration increases and attaches to cdks
cdk has an extra phosphate attached, preventing it from activating the cycle
G2
phosphate group is removed and activates cdk
m phase
cyclin degrades and cdk becomes inactive once division begins
G1 checkpoint
controlled by growth factors
hormones promoting the cycle like gas
tumor suppressors
restrict cell division like brakes
p53: DNA repair
Rb: prevents G1 from transitioning to S-phase
E2F - activates s-phase
must be held back until cell is ready
growth factor produced cyclin and E2F
Rb inhibits e2F
cyclin binds to cdk, which is inhibited by phosphate
phosphate is removed from cdk by an enzyme, cdk removes phosphate from ATP and attaches it to the Rb and inactivating it
once rb is inactive, E2F is released and kicks off the cycle
Cancer
caused by too many growth factors, too much phosphate enzyme, too much e2f
also by too much cyclin or mutated Rb
cancer is many diseases caused by uncontrolled cell division
invades nearby tissue and metastasizes
tumor - mass of uncontrolled cells
benign: noncancerous and noninvasive mass
malignant: metastasizing cells
driver genes
protooncogenes - promote cell growth and division by coding for growth factors
oncogenes - mutated alleles causing uncontrolled division
too many of either of these cause cancer
tumor suppressors also can mutate or be broken, causing cancer
Growth Factors
tell the cell to create e2f and cyclin
RAS - gene involved in many cancers
part of signal transduction pathway that tells cell to produce e2f
when mutated, RAS never inactivates and/or tells cell to activate without growth factor
p53 - cell cycle control and DNA repair
transcription factor
DNA damage sets off signaling pathway, p53 tells nucleus to stop cycle until the dna is repaired
defective or missing p53 leads to uncontrolled division
Genetics
one gene mutation usually isnt enough to cause cancer
one oncogene and many tumor suppressor defects must be present
genetic predisposition: increased likelihood of developing a specific cancer
individuals inherit one broken copy and only need to have one more mutation to develop cancer
BRCA: two copies of every gene, individual inherits one of them, it only takes one more mutation to get cancer
environmental factors
carcinogens - substances proven to cause cancer
tobacco, alcohol, UV, pollution
cancer is treated with surgery, chemo, radiation, targeted therapy and immunotherapy