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BIO 3090 > FINAL > Flashcards

FINAL Flashcards

(59 cards)

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1
Q

Cell wall vs extracellular matrix

A

cell wall- takes the mechanical load in plants, in all plant cells

extracellular matrix- takes the mechanical load in animals; depending on the tissue it may be different
ex ECM is extensive and tough in bone/tendon ECM is scanty in muscle/epidermis

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2
Q

extracellular matrix is made by what

A

excretions of cells

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3
Q

cell junctions

A

linking cells together

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4
Q

Primary layer of cell wall

A

inside layer mainly pectin

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5
Q

secondary layer of cell wall

A

outside layer mainly cellulose

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6
Q

what is the driving force of plant growth

A

water pressure/turgor pressure

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7
Q

composition of cell wall

A

made of pectin;plasma membrane and cellulose

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8
Q

roll of cellulose in cell wall

A

determines type of tissue the cell wall functions as
for example if it needs to be wood, ligin consitutes the cell wall
for leafs it is made of another cellulose alloy with waterproof properties

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9
Q

how does orientations of cellulose microfibrils influence the shape of a plant

A

the orientation of cellulose microfibris influences the direction the plant grows

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10
Q

how is cellulose made

A

cellulose synthase complex are imbedded in the plasma membrane and attached to microtubules by adaptor proteins
as the cellulose is being created on the outside of the cell, the synthase walks down the microtubule from the inside creating the cellulose in the same direction as the microtubules

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11
Q

ECM of connective tissues vs muscle/epidermis

A

biggest distinction between tissues-connective and all the rest tissue

connective/epithelial=lots of ECM, takes mechanical load
nervous/muscular=less ECM, cells joined together carries load themselves

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12
Q

cells in connective tissue

A

cells in connective tissue is like raisins in a pudding

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13
Q

collagen properties

A

gives cells high tensile strength

40+ collagen genes & 25% of proteins in mammals

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14
Q

what is collagen fibers made of

A

a single collagen polypeptide chain
a triple stranded collagen molecule 1.5nm
then a collagen fibril 10-300nm
then a collagen fiber. 5-3 microm

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15
Q

location/functions of osteo/fibroblasts

A

osteo-bone
fibro-skin tendon etc

for both it is to create more tissues- eventually become embedded
can involve in scarring
can excrete a protease to breakdown ECM to move through it

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16
Q

how is collagen created

A

created intracellularly in vesicles called procollagen

it is expelled from the cell then a proteinase cleaves off terminal ends which activates self assembly into collagen fibers
this activation occurs OUTSIDE OF CELL

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17
Q

how does collagen get oriented in cells

A

the collagen creating cells orient it once expelled then rearranging it

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18
Q

Ehler Dahles syndrome

A

super stretchable skin ( hyperelstica)
lack of enzyme that converts procollagen to collagen
defects in collagen breakdown lead to diseases like arthritis/cancer

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19
Q

how do integrins attach to collagen

A

an integrin dimer in inbedded into the plasma membrane which is attached to proteins and actin inside the cell

fibronectin is an extra cellular attachment protein which attaches to collagen

once attached fibronectin and integrin attach connecting collagen to the cell

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20
Q

structure of glycosaminoglycans (GAGs)

A

bottle cleaning brush

Covalently link to core proteins to form proteoglycans
Bone = mostly collagen
liquid in eye = mostly GAGsConcentration of GAGs verses collagen gives ECM its consistency

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21
Q

functions of epithelia

A

protective barrier
absorbe nutrients
export waste
receptros for signals

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22
Q

4 types of epithelia

A

stratified-like bricks on top of one another (SKIN)
Columnar
cuboidal
squamous

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23
Q

basal lamina

A

thin tough ECM made of special collagen (Laminin)

laminin allows adhesive sites for integrin molecules from basal membranes and other tissues

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24
Q

how are epthelial cells polar

Study These Flashcards
A

the apical and basal ends are different
for example the gut cells intake nutrients on one side, and export them to a different tissue on another, these are different processes

25
structure/function of tight junctions
seals neighbor cells together with occludin and claudin proteins mkaes it hard for water soluble molecules to not leak as easy this makes its so that the outside of the cell isnt the same concentration of those molecules as the inside of the cell
26
adherin junctions
joins actin filaments of 1 cell to another the actin filaments/cytoskeleton have linker proteins attached to cadherin proteins on the outside of the membrane. The cadherin attaches to the cadherin on the outside of another cell allowing for the mechanical junctinon of 2 cells allowing for contraction
27
desmosome
joins intermediate filaments of 1 cell to its neighbor keratin filaments attached to anchor proteins (cytoplasmic plaque) the anchor proteins are attached to cadherin which attach to the exact same thing from another cell
28
hemidesmosome
intermediate filaments attached to anchor protein attached to cadherin, which attach to another cell, but not the same subunit
29
gap junctions
2 cells connected.by somewhat of an ion channel joining the 2 membranes the channel is called a connexon can be opened or closed quickly
30
plasmodesmata
links cell wells, these are lined by plasma membranes therefore all membranes are linked together small and large molecules can move in these
31
tissue stability factors
cell communication- monitors environment for signals from other cells to adjust its behavior accordingly (proliferation) selective cell adhesion- makes sure correct cells communicate cell memory- gene expression patterns enacted during first development are maintained
32
cell turn over rates of skin bone blood intestine tissues
skin- continueous pushing cells outward as skin sheds bone- 10 years blood- 120 days intestines- 3 to 6 days
33
mixtures of cell types for skin
epithelium of epidermis - dead skins cells sluffing off (keratinocytes melonin) dermis- blood vesles nerves, (lymphocytes, collagen, macrophages) inner dermis- (fibroblasts, elastic fibers) hypodermis- fatty tissue
34
how do stem cells produce an unlimited supply of differentiate cells
the stem cells provide 1 daughter stem cell and 1 precursor stem cell which when dividing differentiates its daughter cells
35
cells dividing in the gut vs skin
in the gut they divide in the crypts of cell folds, the new cells slide up one spot, then as cells divide they move up more and more spots until they reach the top of the fold which they then die in skin, the cells divide at the bottom layer, pushing all the old skins cells up a little bit until the cell reaches the top and dies and is replaced by another cell
36
appearance distribution abunance of stem cells
non descript appearance held in resident tissue along with differentiated progeny cells precent in small numbers
37
example of stem cell giving rise to other cell types
hemopoietic stem cell in bone marrow create RBC WBC and everything in blood
38
Embryonic stem cells can do what
embyonic stem cells can turn into anything and are therefore called pluripotenet
39
obstacles using embryonic stem cells to regenerate damaged tissues like diabetes/parkinsons
immune rejection | ethical concerns
40
induced pluripotent stem cells vs embryonic
induced stem cells come from any cell in the body once given certain transcription regulators, can do anything an embryonic one acn embryonic comes from an embyro
41
iPS cells being studied for what
these cells can create large swaths of tissue able to be tested on for drugs and such
42
singaling mechanisms maintaining organization of systems like intestines
Wnt proteins- when active cells proliferate | when not active cells dont proliferate
43
2 heritable properties of cancer
proliferate in defiance of normal contraints | invade and colonize territories for other cells
44
benign, malignant, metastasis tumors
benign-proliferate but dont spread malignant- can proliferate into other tissues metastases- forms secondary tumors in other sites of the body
45
epidemiological evidence for environmental cancer
HPV & Cervical cancers smoking & lung/bladder cancer obesity
46
sources of mutation that causes cancer
radiation and chemicals
47
passenger vs driver/cancer critical mutations
passenger mutations do not cause cancer | driver/cancer critical mutations cause cancer
48
passenger vs driver/cancer critical mutations
passenger mutations do not cause cancer | driver/cancer critical mutations cause cancer
49
why is cancer mostly affect old people
because thats usually when the accumlulation of mutations from throughout life cause cancer
50
how does genetic instability contribute to cancer
genetic instability increases rate of cancer creation because fewer mutations are needed to create it
51
how do tumors evolve through repeated rounds of mutation/natural selection
each mutation doesnt cripple the cell it may give it a slight advantage over the other cells eventually it gets another mutation and another until it becomes cancerous
52
characteristics/advantages of cancer cells over normal cells
1) reduced dependance for survival on other cell signals 2) can survive levels of stress that would normally cause apoptosis 3) can proliferate indefinatly due to telomerase activity 4) genetically unstable can mutate more 5) invasive of other tissues 6) avid for nutrients/less oxygen dependant 7) can survive in weird locations 8) can influence behavior of other cells to advantage itself
53
key regulatory pathways usually mutated in all cancers
cell proliferation DNA damage responce cell growth cell survival
54
tumor suppressor genes for cancer
usually loss of function recessive stops regulatory pathway that suppresses cancer
55
oncogenes for cancer
dominant mutations comes from protooncognes gain of function
56
how does loss of APC contribute to cancer
has 1 mutant copy and 1 nonmutant copy, eventually it can mutate and cause cancer the 1 copy mutation causes polyps in the intestines can cause metastatic cancer because 1 mutation causing cancer is more likely than 2
56
how does DNA damage/faulty cell cycle control contribute to cancers downfall w treatements
treatments can try to make DNA less stable making the genome in the cancer fall apart treatments can also destroy quickly dividing cells like cancer killing them Cancer cells survive by relying on alternate types of DNA repair mechanism Drugs that inhibit these alternate DNA repair mechanisms will selectively destroy cancer cells
56
antibodies and killing cancer
antibodies can kill cells w surface molecules found | oncogenes
56
product of oncogene can be targeted to kill cancer
gleeve block the kinase activity

BIO 3090 (5 decks)

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