4: Fungus Flashcards
MHC 1
found in ALL cells (even professional APCs)
for pathogens that get into cytosol of cell
MHC 2
only B cells, dendritic cells, and macrophages
professional antigen presenting cells
CD8 T cell recognition… Class one
antigen presention
peptide in binding pocket of MHC
MHC with peptide binds to T cell receptor binding pocket (random VDJ)
ONLY after bound to MHC, T cell generates something that recognizes the peptide
CD8 recognizes
peptides bound to MHC class 1
CD4 recognizes
peptides bound to MHC class 2
CD4 T Cells HELP. how it works
APCs bring in the pathogen, digest it, put on MHC2
MHC2 recruits CD4
what if the pathogen gets IN the cell?
CD4 and MHC 2 cant be used, use MHC1 for presentation
How MHC 1 works
pathogen gets into cytosol
MHC1 is in lumen of ER (so basically outside cell), so fusion will put MHC1 on surface
proteosome injgests pathogen and changes to peptide prep center when we have interferon. This lets proteosome load the MHC1
CD8 and NK
similar, both kill BUT
CD8 is adaptive
NK is innate
review slide 9
review slide 9
what happens after activation
APCs generate 3 signals
signal 1 after activation
T cell receptor and peptide/MHC dock
costim. from CD4 or 8
strong binding=recognition
signal 2 after activation
check for T cell to know that its a healthy antigen presenting cell
signal 3 after activation
proinflammatory cytokine released by APC
signal tells T cell what type of organism the antigen came from (based on what innate receptors were activated along they way)
so that future contact with that antigen will have a more specific response
classes of CD4 T cells
Th1 Th2 Th17 Tfh Treg
Th1
for bacteria
activate macrophges
Th2
for parasites and fungi
activate mast cells
Th17
in mucous membranes, bacteria
activate neutrophils
Tfh
B cell differentiation
Treg
responsible for NOT activating
ingestion of food, we ingest a foreign antigen this way
we recognize it neither as self or pathogen
tolerance
problems with this cause chrons disese… immune responses to food
Adaptive immunity can be
natural or artificial
each of these can be active or passive
Natural active immunity
antigens enter body
body makes antibodies
become immune
Natural passive immunity
antibodies pass from other to fetus by placenta or to baby from milk
mother makes antibodies, not baby
no activity required
Artificial active immunity
antigens introduced by vaccine
body makes antibodies
Artificial passive immunity
pre-made antibodies injected into serum
antibodies from a different person that were made when they were sick
used for ebola treatment a bit
Meiosis
production of haploid gammates for sexual reproduction
sexual reproduction good because
it improves group genetics
how many chromosomes do humans have?
23, 2 copies of each
one copy from mom, one from dad
come together when sperm and egg combine (haploid)
haploid cells
only ONE copy of each chromosome
23 chromosomes total, not 46
How is it that grandparents about equally contributed to your genetics?
sexual recombination
sexual recombination
chromosomes line up and recombine
cross-over between chromosomes generates new combo of genes
4 eggs made by meiosis, each has different combo of parental genes
why sexual recombinatation
allows sexual species to store genetic info in multiple individuals
ability to solve problems and let the species survive
why humans and chimps arent the same species
we have 23 chromosomes, they have 24
sexual dimorphism
2 sexes evolved
advantages of hermaphrodites (worms)
both individuals can become impregnated
any encounter can be productive… two males meeting would not be. But if sexes aren’t different, any 2 individuals meeting can produce offspring
advantages of sexual dimorphism: colonies (bees and ants)
colonies are all females, males go away as drones
drones come to new colonies and bring new genetic material
advantages of sexual dimorphism: angler fish
not enough food at bottom of ocean for a lot of big fish
so males are tiny and don’t “eat”, the feed off female blood. attach to female just to release sperm when she releases eggs.
male is a parasite
sexual vs. asexual reproduction
review slide 24
Fungal mating types
more than 2 sexes
advantages of multiple sexes (fungi)
ability to determine closeness of genetic relationship
pheromone-phermone receptor parings
how fungi tend to pick mates… mate if different phermones
as many sexes as there are alleles
Shome fungi are HOMOTHALLIC
can mate with other or self
heterothallic fungi
only mate with different cheomtype
(non-self mating)
want recombination with something not genetically similar
Fungi are
eukaryotic
saprophytic
aerobic or sometimes facultative anaerobic
produce spores
saprophytic
absorb food instead of eating or photosynthesizing
fungi you can eat
alcohol, bread, some mushrooms
cell wall of fungi
made of glucans, mannans, chitin
3 layers
parts of fungi
nucleus, mitochondira, organelles
fungal spores
not tough like bacterial
single celled fungi
yeasts
bigger than bacteria
mulitcellular fungi
molds, fleshy fungi
hyphae structure
yeast division types
fission: divide down middle
budding: babies bud off the sides
hyphae structure
primary structure. longs tubes filled with cytosol
cells not divide like in humans
some septated: units like cells with holes that let cytosol move between them
some just contnuous (coenocytic)
hyphae and communication
secretions of organelles diffuse through cytosol that movement between “cells”
Characteristics of molds
thallus (body, reproductive)
Septa: serpate hyphae, coenocytic hyphae (no septa between cells)
multinucleated
reproductive or vegitative hypahae
Budding yeast
asexual asymetrical division. leaves scars can only bud 24 times different ways budding can happen: diploid and haploid
Feromones and Feromone receptors
allow to determine genetic relationships between haploid cells
lifecycle:
2 HAPLOID groups find each other: PAIRING
produces its own pheromones, and has pheromone receptors for the other kind
move towards eachother and fuse to make DIPLOID
DIPLOID can undergo meiosis or mitosis
review slide 34
review slide 34
