BG4 Flashcards
colonial and multicellular
colonial: multiple cells not specailised
multicellular: multiple specialsied cells
evo of multicellularity in euraryotes
evolved 6x in eurkartores: animals. fungi, algae (RGB), land plants
evo of multicellualrity volocine
shows a series of chomplexity from single cell chlamydomonas to gonium which is often a sheet to volox which is large with thousands of cells, inc. specailised germ and somatic
myxcoccus
gram neg bacteria, feed on other bacteria in packs
food used up, they glide towards each other and form mounds of cells and fruiting bodies with specialised cells
most cells die, only few form myospores which germine anad undergo vegetative growth adn swam again
Dictyostelium
multicellular slim mould
single cells live seperately in soil eating bacteria
when bacteria runs out, one of these cells releases cAMP which stimulates other cells to release it
this causes the cells to aggregate together and form a motile slug, slugs can join together or go through one another.
eventually the slug stops and produces a stalk witha fruiting body on the top.
benefits of multicellularity
- increase body size (anti-predation, economic benefits)
- cell specialization
- increased efficiency of coop feeding.
costs of multicellularity
- reduced growth rate (not all cells replicating)
2. cheating
experimental evolution of multicellularity
take unicellular saccharomyces; grow in a shaking incubator, remove, allow to settle, select/pipette the yeast that has settled most quickly
- yeast that glom together settle faster
propogate each day
experimental evo of multicellularity results
in 60 days get a multicellular snowflake phenotype
genuine multicellulairy with some cells being apoptosed to produce holes that give optimal biophysical structure such that they sink quickly.
dictylostelium Hamiltons theory
stalk composed of 20% of cells - cells dont produce cells but die = hamiltons theory of altruism
cheaters in dictylostelium
some genotypes evade forming stalks adn preferentially form spores that are dispersed.
cheating mutations in dictylostelium
- some eat other preventhing them becoming spores
- some divide faster/inhibit division of others
- some dont secrete cAMP
- some ignore lateral signals specifying stalk
- some evidence cheaters become disproportionate lead to extinction as they fail to diversify and make slugs or pleiotropy prevents proliferation
sponges avoiding invasion
evolved system of self and non self recognition
- take three species of sponges rob
- grind them into soup, sponges disintegrate into individual cells
- then form species specific aggregates and reform into sponges.
sponge aggregation factor
sponge self/non-self recognition is due to cell-suface glyconectin
- each AF i composed of many glycoproteins arranged in a sunburst configuration that bind to specific receptors on cell surface
- core proteins show distant homology to other cell membrane proteins but nothing like it is found in other metazoans
examples AF
MAFp3 carrying g200 glycan
MAFp4 carrying a g-6 glycan
ascidians
sponge like chrodates also compete for space, risk of invasion by conspecifics *(same species)
ascidian conspecifics risk of meeting
either fuse or reject each other
fusion between two colonies of botryllus invader can replace not only somatic cells but germ cells of invadee, so propagates invaders germ cells
fusion of ascidian
botryllus only fuses with genetically similar colonies
genetic recognition is regulated by fusion histocompatibility complex. FuHc locus
FuHC`
highly polymorphic posses many codom alleles
colonies that guse have atleast one FuHC in common
colonies that reject each other have none.
FuHC homology
hasnt been cloned yet
but thought to resemble MHC system
cancers
cheater cells
mutations evolved leading to single cell clonal organisms,
MHC
genes encode cell surface receptors that bind to foreign peptides and present them to T cells
many MHC genes, encoding proteins of several classes, some enormously variable with 100’s of alleles
enable distinguishment of self from not self
MHC transplants and contagious cancers
MHC are the reasion behind trannsplant rejection and reason cellular rather than viral cancers arent contagious
CVTS
canine venereal transmissible sarcoma.
- cause via sex
- originated 10,000 years ago from wold/husky like animal
- LCA lived 500 years ago
- host manipulation - infected dogs secrete for sex pheromone
- suggetion evolved from myeloid cells possilbly macrophage lineage (can expression MHC classes)
CVTS mitochondria
periodically acquired new mitochondria from hosts, multiple endosymbiosis events
perhaps because its clonal so mutations accumulate and disable mitochondria forcing it to get new ones
sequenced cvts
- massive copy no. variation
- nearly 50% of genes have NS subs. - inc cancer genes myc, erg.
- 3% of genes are disabled by mutation - presumably genes involved in multicellularity.
immunosuppression strategies of ctvs
does not metastasize or kill host, regresses after a while
invasion phase has low MHC1 and 2 expression
secretes lots of TGF which inhibits host T-lymphocytes and NK cells
TGF also downregs MHC in both host and tumour
DFTD
- tasmanian devil
- catch by scratching/fighting
- transcriptomics show derived from schwann cell
- karyotype of tumour cells is conserved by diverged from normal devil cells
- driving devils to extinction
features of animal multicellularity
- specialisation of cell types - cell and tissue specific TFs
- allorecognition and innate immunity - immune system molecules MHCs
- regulated cell cycling and growth - cell cycle and genes and GFs
- PCD - PCD pws.
- cell/cell and cell/matrix adhesion – architectural elements
- developmental signalling and gene reg/regional specificaiton via signalling molecules and regional TFs
hamster transmissible cancer
- reported in colony of syrian hamster, can be transmitted by mosquito A. aegypti bite
human transmissible cancer
rare
malignant fibrous histiocytoma contracted from patient by surgeon when he injusred his hand during an operation.
though tumour escaped immune destruction via changed to MHC or abscence of immunogenic tumour antigens
cross species cancer transmission
41 yearold man with HIV
tumour found to originate from dwarf tapeworm H. nana
parasite to host cancer transmission.
hypothesized mutation causing continued proliferation in immunosuppressed host allowed somatic mutations to occur in parasite stem cell population leading to malignant transformation
bottlenecks and transmission
bottlenecks increase risk of cancer
loss of MHC diversity, higher risk of tumour transmissible tumours
both hamsters and devils tumours spread among animals with little gentic diversity
CVTV variants on the other hand evolved immune evasion enabling them to cross MHC barrier
