Cell Communities1 Chapter 20 Key topics Structure & function of -- the extracellular matrix -- cell...
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Transcript of Cell Communities1 Chapter 20 Key topics Structure & function of -- the extracellular matrix -- cell...
Cell Communities 1
Cell CommunitiesChapter 20
Key topics
Structure & function of-- the extracellular matrix-- cell junctions
Tissue organization
Properties of -- Stem cells-- Cancer cells
Questions in this chapter you should be able to answer:
Chapter 20: all
Cell Communities 2
Extracellular Matrix – I Plant cell wall
Compositioncellulosehemicelluloselignin
OrganizationMiddle lamella1O wall2O wall
Plasmadesmata
Cell Communities 3
How are cellulose fibers synthesized and oriented?
Cellulose organizationCellulose synthase
-- pushed forwardMicrotubule tracts
– constrain movement
Cellulose fibers Microtubules
Cell Communities 4
Animal tissue organization
EpitheliaExtracellular matrix
-- Basal lamina-- Connective tissue
Epithelia have polarityTight junctions separate
apical vs basal surfaces
apical
Cell Communities 5
What are the 1O components of the ECM?
CollagensProteoglycans
Collagensstructure (Glc - X - Y)
X often prolineY often hydroxyproline
functionorganizationmany types
Gelatin
ScurvyVitamine-Cprolyl-hydroxylase hydroxyproline
Fibroblasts
Collagen
Cell Communities 6
What are proteoglycans?
Polysaccharide core (hyaluronate)+ Protein linkers+ GAG branches (glucoseaminoglycan)
GAGs-- Repeating disaccharides-- cationic-- e.g., Chondroitin
Functionshydroscopicswelling pressureinfluence cell migration
Cell Communities 7
How are cells linked together and to extracellular matrix?
May involveCytoskeleton
and componentsOf extracellular matrix
Cell Communities 8
What creates Cell-Cell linkages?
Cadherins mediate cell-cell linkage-- many types: C-, E-, P-, T- cadherins-- “homophillic” binding
Can be connected to cytoskeletonDesmosomes – intermediate filamentsAdherin junctions – actin filaments
Classic newt embryo experiment -- Townes and Holfreter (1955)
(simplified)
Cadherins
Cell Communities 9
Linkage to the ECM are also important
Integrins – mediate linkages between cytoskeleton and ECM
Also can be connected to cytoskeletonHemidesmosomes – intermediate filamentsContact Adhesions – actin filaments
linkages are ‘responsive’
Question 20-4Why are these linkages more common in fibroblasts, and desmosomes and adherin junctions more common in epithelial cells?
Cell Communities 10
How does tissue renewal occur?
Cell division vs stem cellse.g., Liver vs skin
What are the properties of stem cells?
Self renewal
Developmental commitment
Precursor terminally differentiated
Cell Communities 11
Somatic vs EmbryonicStem (ES) cells
Somatic – tissue specific-- degrees of commitment
-- multipotent vs unipotent
ES – any developmental fate-- must follow developmental pathway
-- else neoplasm
Cell Communities 12
How do somatic stem cells renew skin?
Skin structure-- stratified epithelium
Epidermal stem cells
Example of a stratified epithelium
Cell Communities 13
How do somatic stem cells renew intestine?
intestine structure
Epithelial stem cells
How is pattern of tissue regeneration different than for skin?
-- Is intestinal epithelium simple or stratified?
Cell Communities 14
Stem cell biotechnology
Tissue repair-- CNS injury-- burns-- disease (macular degeneration)
Organ replacement?-- in vitro regeneration
ES-cells
Cell Communities 15
Why do cells become tumorous?
Which type of cancer gene causes loss of cell division control?
Which type of cancer geneleads to genetic instability?
Which type of mutation requires two altered alleles to exert it’s effect?
-- How does LOH overcome this constraint Meningioma karyotypeLOH - #17 (Loss Of Heterogenecity)Aneuploidy - #s 9, 7, and 20Translocation/duplication - #s 2 and 6
Cell Communities 16
How does loss of genetic stability lead cells to become cancerous??
Benign tumor vs Malignant tumor vs Cancer
Evolutionary process
Lost dependence of extracellular regulation-- checkpoint failure
Loss of ‘mortality’ (e.g., telomere renewal)
Activation of genes for motility and invasiveness-- cell junction breakage-- cytoskeletal changes
Altered metabolism-- higher glycolysis, less Krebs – why?
Abnormal adhesion proteins-- cadherins, etc-- growth in new areas