Flashcards in Histo exam 1 Deck (83):
What is cardiolipin?
In inner mito. membrane, makes membrane impermeable to electrons and protons!
anchors ACTIN by CATENIN and VINCULIN; Ca2+ dependent actions between cells through CADHERIN PROTEINS
use CATALASE to break down long chain fatty acids to acetyl coa and then to hydrogen peroxide, replicate by fission
intermediate filament for epithelial cell?
phospholipid polar region made up of:
+ choline and - phosphate
cholesterol forms microdomains called:
lipid rafts- lots of concentrated cholesterol important for cell to cell interactions
Tay Sachs- defect in ganglioside metabolism, missing hexosaminidase, affects CNS neurons
how does the glycocalyx protect the cell?
have as strong negative charge on outer surface to block infection
movement of macromolecules and particulate matter across cell membrane is called:
endocytosis and exocytosis
3 types of endocytosis:
receptor mediated endo.
phagocytosis- eat big stuff
how does pinocytosis work?
bulk fluid uptake into CLATHRIN coated vesicles, vesicles pinch off by DYNAMIN
how does receptor-mediated endo. work?
LDL receptor on membrane pick up LDL molecules, fall into clathrin coated pit, pinch into a vesicle, acidity causes receptor and ligand to unattach, dealt with by lysosome
how does phagocytosis work?
NOT CLATHRIN DRIVEN! caused by changes in active cytoplasm- done by macrophages and neutrophils, rearrange actin cytoskeleton, phagosome, stuff binds to receptors on cell membrane
2 types of exocytosis
1. regulated pathway: controlled by specific stimulus (hormones cause calcium to trigger zymogen granules released to small intestine)
2. constitutive pathway: replaces membranes and membrane proteins as well as secreting materials synthesized by the cell (mucous secretion by goblet cells)
RER : SER
flattened sacs: tubes
membrane synthesis, make steroid hormones, Ca homeostasis (sarcoplasmic reticulum), detox of lipid soluble drugs, metabolic waste and ingested toxins by cytochrome p450 system
makes integral and secreted proteins, 1st site of post-translational modification
ribosome size? translation?
12nm wide, 25nm long, signal sequence binds to signal recognition particle which binds to SRP receptor on RER, keeps translating, signal peptidase cuts off signal sequence
trans face: sort/packages stuff into:
1. non-clathrin coated vesicle to PM
2. clathrin coated vesicle
3. lys. enzymes for the lysosome gets mannose6p since lysosome has a m6p receptor, also has clathrin coating
lysosome size, function
<1 micrometer, irregular shape, have acid hydrolases, come from trans golgi network,primary lysosome + late endosome = secondary lysosome
lysosomes and osteoclasts
lysosomes release hydrolytic enzymes in extracellular space that osteoclasts use to do bone remodeling
autophagy and heterophagy
thing that eventually combines with lysosome is from cell (autophagy) or outside cell (like a bacteria that was phagocytized) heterophagy
what are lipofuscin residual bodies?
stuff that can't get let out are suck there, build up in cell. have secondary lysosome action
pompe lysosomal storage disorder?
no glucosidase, accumulate glycogen, bad for heart
hurler lysosome storage disorder?
no L-Iduronidase, accumulate dermatan sulfate, affect skeletal system
Niemann-Pick lysosomal storage disorder?
no sphingomyelinase, accumulate sphingomyelin, affect CNS oligodendrocytes
.2 micrometer, fission, aka microbodies
have CATALASE and other oxidative enzymes to break down long fatty acid chain to acetyl coa to hydrogen peroxide
.5 micrometer x 7 micrometer, make ATP, slef replicate
has krebs cycle enzymes, matrix granules important for binding Ca2+, circular dna and own mRNA, tRNA, ribosomes
mito. inner membrane
ATP synthase protein complex, ETC enzymes, lots of CARDIOLIPIN- makes membrane impermeable to electrons and protons
what stuff counts as INCLUSIONs?
glycogen granules, lipid droplets, pigment granules (lipfuscin, melanin), crystalline inclusions
nuclear pore complex?
allows free passage of ions/molecules < 60kDa
bidirectional ACTIVE transport of big stuff
-nuclear localization (importin) signals
-nuclear export signals (exportin)
chromatin 2 types:
euchromatin: <30 nm, dispersed, transcriptionally active
heterochromatin: condensed, inactive
where rRNA is made, ribsome subunits assembled, VERY acidic/basophilic
inner membrane supported by nuclear lamin A,B,C
outer membrane continuous with RER
actin, maintain cell shape, cell cortex, cytoplasmic streamingm cell motility (treadmilling to make pseudopodia), muscle contraction, cell division (make cleavage furrow), add at + end, decrease at - end
form nuclear lamina, anchor nucleus and other organelles, tension bearing elements, structurally homologous but biochemically distinct
cytokeratin intermediate filaments let epidermal cells/skin resist stress, mutation in CYTOKERATIN --> fragile skin, blistering
cell shape (compression resisting girder), organelle movement (kinesin, dyenin), mitotic spindle, cilia/ flagella
long straight rigid: alpha/beta tubulin dimer
minus end in microtubule organizing center (MTOC), polymerize and depolymerize at (+) end
kinesin and dynein
ATPases: transport membrane bound organelles along microtubules
KINESIS, anterograde: - -> +
DYNEIN, retrograde + -> -
Why have a PAS stain of microvilli?
has lots of carbs, glycocalyx, actin based structure
microvilli size? function
1-2 micrometer long, 80 nm diameter, actin cytoskeleton, non-motile, increase SA
cilia size? function? structure?
8-10 micrometer long, .25 micrometer diameter,
move fluids over cell surface, anchor to basal body, DYNEIN-dependent hydrolysis of ATP, AXONEME- microtubulues in 9+2 organization
no dynein arms in cilia, respiratory problems, mucus pool at bottom of lungs, sperm problems
is stereocilia real cilia?
NO, long microvilli, in testes and hair cells
is kinocilia real cilia?
YES, non-motile cilia, 9+0 axoneme, hair cells
tight junction, complex of OCCLUDIN and CLAUDIN, prevent water soluble molecule movement btw. cells and movement of integral proteins
--> bad ones lead to leaky gut syndrome
adhesive by DESMOGLEIN and DESMOPLAKIN, intermediate filaments anchor to it
CONNEXONS channels made of 6 connexin subunits, let ions/small molecules pass btw. cells, couple cells electronically and metobolically
basement membrane and cell-to-extracellular matrix connections
hemidesmosome--> basal lamina (lamina lucida, lamina densa) -> reticular fibers
LAMININ, TYPE 4 COLLAGEN, ENTACTIN, PERLECAN
for support, filtration, adhesion
transmembrane protein (alpha/beta heterodimer), couple to actin cytoskeleton, alpha chain mediates adhesion by binding to short recognition sequences on ECM molecules like LAMININ, FIBRONECTIN, COLLAGEN
-important in SIGNAL TRANSDUCTION
autoimmune disease against parts of desmosome/hemidesmosome
-epidermal blistering and loss of extracellular fluid
inherit defect in type 4 collagen, filtration problem so blood goes in urine (hematuria)
cell cycle control: extrinsic factors
nutrients, growth factors
cell cycle control: intrinsic factors
cell senescence, accelerated aging
Werner's- mutation in gene encoding DNA helicase
Progeria (Hutchinson-Gilford) - mutation in intermediate filament that lines nuclear envelope
cyclins in interphase
G1 -> S: cyclin D and E
S->G2: cyclin A
G2-> M: cyclin B
chromosome condense, kinetochore go on centromeres, centromere go to poles, spindles start to form
nuclear envelope breaks down, microtubules attach to kinetochores, chromosomes begin to migrate
sister chrom. separate, cleave furrow begins to form
spindle microtubules begin to depolymerize, nuclear envelope forms around daughter nuclei, chromosomes begin to decondense and nucleoli form, cleavage furrow deepns
which cell cycle anti cancer drugs disrupt mitotic spindle formation?
vincristine/colchicine destabilize microtubules
taxol stabilize microtubules to prevent from moving
which anti cancer/cell cycle drug inhibits DNA synthesis?
5-fluorouracil/methotraxate block formation of deoxynucleotides
cytosine arabinoside- analog of cytosine that blocks DNA replication
What are the 5 steps of meiotic prophase?
1. leptotene- condense
2. zygotene- pair
3. pachytene- recombination
4. diplotene- oocyte dormant til puberty here, coil
5. diakinesis- recondense, nucleolus and nuclear envelop disappear
nondisjunction in 1st meiosis, homologues didn't get pulled apart
What is the giesma stain?
chromosome banding in karyotype- general organization of genes within each chromosome
chronic myelogenous leukemia- philadelphia chromosome?
dna between chromosome 22 and 9 get swapped, wild replication of cells in bone marrow
how long does apoptosis take?
physiological examples of apoptosis
embryo development (delete webs)
cell turnover (intestinal crypt)
t-cell conal deletion
normal involutional process (breast, ovary, endometrium)
atrophic processes (prostate)
apoptosis examples in pathology
atophic process (kidney, liver)
immune-mediated cell killing (rejection, graft vs. host)
cellular injury (radiation, chemo, toxin)
disease and increased apoptosis
aids, neurogenerative disorder (parkinson, alzheimer, amytrophic lateral sclerosis, retinitis pigmentosa, cerebellar degeneration), aplastic anemia, alcohol toxin liver disease, ischemic (heart injuries)
HEART AND BRAIN
disease with inhibition of apoptosis
cancer, autoimmune disorders, viral infections (herpes, pox, adenovirus)
mechanisms of apoptosis
1. organelle dysfunction (intrinsic)
2. DNA damage
3. death receptor activation (extrinsic)
4. abnormal protein folding/ accumulation
apoptosis: organelle messed up!- intrinsic
BAX activated, pokes hole in mitochondria membrane, AIF, Cyt. C, APAF-1 come out --> CASPASES --> nuclear fragmentation
extrinsic apoptosis pathway
cell death receptor activated at cell membrane, caspase cascade leads to apoptosis
necrosis affected diseases
neurodegenerative, cerebral ischemia, heart disease
what are triggers of necrosis?
acute energy depletion, trauma, harsh environment, extrensive DNA damage
bother ion homeostasis (increase Ca, Na, Mg, Zn, acidosis, degenerins for animals)
protein degradation- lysosomes (cathepsin, hydrolase), CALPAINS, caspase
autophagic vacuoles accumulate in cells, type 2 cell death (lysosomal)
autophagosome (membrane bound structure with damaged organelle) merge with lysosome and gets digested
autophagy occurs in
development, differentiation, tissue remodeling, cancer, liver disease, muscle disease, neurogenerative disease, infection
preventing cell death
Ca2+ blockers, caspase inhibitor, protease inhibitor, glutamate receptor antagonist (memantine), growth factors (BDNF), cytokines, antioxidants
FUTURE: gene therapy (bcl2 gene transfer), natural caspase inhibitor, understand hibernation, anti-apoptotic molecules (anti-p53)
cell death regulators
p53, bcl2, cell cycle genes, fas ligand, cytokine, proteosome, mitochondria, lysosome, calcium