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Fig. 1.11

Fig. 1.11

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Fig. 1.11. Heterochromatin = too compacted, transcriptionally inactive. Nucleus: structure and function. nuclear envelope. Nucleolus. Nucleoplasm. Euchromatin = can be transcriptionally active. Nuclear envelope and lamina. cytoplasm. N. lamina. Nuclear pore. heterochromatin. - PowerPoint PPT Presentation

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Page 1: Fig. 1.11

Fig. 1.11

Page 2: Fig. 1.11

Nucleus: structure and function

Nucleolus Nucleoplasm

nuclear envelope

Heterochromatin = too compacted,

transcriptionally inactive

Euchromatin = can be transcriptionally active

Page 3: Fig. 1.11

Nuclear envelope and lamina

Nuclearpore

N. lamina

cytoplasm

heterochromatin

Page 4: Fig. 1.11

Nuclear lamina

Page 5: Fig. 1.11

Lamins are filamentous proteins in the intermediate filament family

Lamin phosphorylation in prophase disassembles the nuclear lamina & allows for nuc. envel. breakdown

Laminins are extracellular proteins, unrelated

Page 6: Fig. 1.11

Nuclear pore

• nuclear localization signals (nuclear import signals)

• nuclear export signals

• highly regulated

Page 7: Fig. 1.11

Mitochondria(on)

outermembrane

innermembrane

DNAmatrix

cristaeribosomes ATP synthase

Page 8: Fig. 1.11

Inner Membrane and matrix

electrontransportsystem

ADP3-

ATP4-

pyruvate

Krebscycle

NADH

ATPsynthaseFADH2

hi [H+]

Antiporter

P04-2 H+

symporter

Page 9: Fig. 1.11

Endosymbiotic theory: Mitochondria are similar to

prokaryotes• Own circular, naked DNA• Own ribosomes - similar to prokaryotic

o e.g. sensitive to same inhibitors• Divide by fission• Double membrane suggests endocytosis

Page 10: Fig. 1.11

Lysosomes: membranous organelles filled with digestive

enzymes• Breakdown

endocytosed materialso Thru’ phagocytosis or

receptor mediated endocytosis

• Breakdown old organelles (residual body)

• Acidic pH

Page 11: Fig. 1.11

Phagocytosis vs. Autophagy

Phagocytosis

Autophagy

lysosomes

Page 12: Fig. 1.11

Membrane trafficking

• RER to cis Golgi• Modified in Golgi

(glycosylation, phosphorylation)

• Sorted at trans Golgi network intoo Lysosomalo Regulatedo constitutive

Page 13: Fig. 1.11

Synthesis of secreted and membrane proteins

Ribosomes

Rough endoplasmic reticulum

Page 14: Fig. 1.11

Rough Endoplasmic reticulum

Page 15: Fig. 1.11

Signal hypothesis: signal peptide, SRP, SRP-receptor,

translocon

SRP = signal recognition particle

Page 16: Fig. 1.11

Smooth ER, lipid synthesis, detox, Ca2+ sequestration

Page 17: Fig. 1.11

Golgi

Page 18: Fig. 1.11

Transport thru’ Golgi cisternae is vectorial

Cis Medial Trans

Page 19: Fig. 1.11

mannose removalN-acetylglucosamine addition MEDIAL

RER retrieval, PO4 on mannose,mannose removal

CIS &CGN

fucose and glucose addition TRANS

sialic acid addition, sorting TGN

Protein modifications occur in steps in the Golgi. The extent of changes

varies.

Page 20: Fig. 1.11

Glycosylation

Karp, Fig. 8.20

Page 21: Fig. 1.11

trans Golgi network

regulatedsecretion

lysosomalpathway

constitutivesecretion

Sorting at the TGN

Page 22: Fig. 1.11

Receptor Mediated endocytosis

Page 23: Fig. 1.11

Plasma membrane & Fluid mosaic model

Page 24: Fig. 1.11

Phospholipids are most common in membranes

PolarHead

Fattyacidtails

Page 25: Fig. 1.11

phospholipids, glycolipids, and cholesterol

Page 26: Fig. 1.11

Thermodynamics drives membranes to form sealed compartments

H2O

Cut open liposome

Page 27: Fig. 1.11

Fluidity means that lipids (& proteins) can “float” in the membrane via

diffusion

Time

Page 28: Fig. 1.11

Three classes of membrane proteins: Transmembrane proteins (a type of IMP)

OUT

IN

Extracellulardomain (ECD)

Intracellulardomain (ICD)

Transmembranedomain

Oligosaccharides - always face out

Page 29: Fig. 1.11

Three classes of membrane proteins: Lipid-anchored membrane proteins

(IMPs)

OUT

IN

Covalently linked to a glycophospholipid.

E.G.: Normal cellular scrapie protein & alkaline phosphatase

Covalently linked to fatty acid

E.G.: ras

Page 30: Fig. 1.11

Three classes of membrane proteins: Peripheral membrane

proteins (PMPs)

OUT

INOr, PMPs could bind to specific lipid heads.

Specific interaction between IMP & PMP

Page 31: Fig. 1.11

IMPs as -helix or -barrel

Page 32: Fig. 1.11

Selective permeability

Page 33: Fig. 1.11

Osmosis causing cell lysis.

Page 34: Fig. 1.11

Four mechanisms by which solute molecules move ACROSS

membranes

Simple diffusionacross bilayer

Simple diffusionthru channel

FacilitatedDiffusion

thru’ passive transporters

Activetransport

Page 35: Fig. 1.11

Membrane Potential Affects Molecular Movement

A. neutral

No effect on inward transport

No effect on outward transportB. cation

Favors inward transport

Opposes outward transportC. anion

Opposes inward transport

Favors outward transport

Page 36: Fig. 1.11

Passive transport by channel proteins: don’t bind solute & can be ligand-, voltage-, or stress-

gated

Page 37: Fig. 1.11

Passive Transport by Facilitated diffusion

• Solute binds transporter protein

• So, transport is saturable

Page 38: Fig. 1.11

Kinetics of carrier-mediated transport

Page 39: Fig. 1.11

Active transport by the Na/K pump or ATPase