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Transport of RER to lysosome - Coggle Diagram
Transport of RER to lysosome
Golgi complex
medial (middle part)
cis
faces the ER
trans
faces the cell membrane
properties
has flattened cisternae
processes and sorting proteins
the vesicles at cisterna tips fuse or pinch off
transport vesicles
components
membrane cargo protein
transverses golgi from the cytosol to the ER
membrane cargo-receptor
allows binding of soluble cargo protein to transport soluble cargo protein
v-snare protein
binds to the s-SNARE protein to cause fusion to membrane
coat proteins
promotes budding of vesicles
soluble cargo protein
protein that free floats in the ER
anterograde transport
RER to golgi
uses COPII vesicles
GTP binding protein recruits coat protein
a conformation change occurs causing the budding off the membrane (creates COPII vesicle)
when near Golgi,GTP promotes dissociation of coat proteins
ATP hydrolysis promotes snare protein disassembly
cystic fibrosis
delta 508 mutates the disassorting system to be unrecognized by COPII proteins
proteins do not go to membrane because it is stuck at the ER
retrograde transport
cis golgi to RER
uses COPI vesicles
ER resident protein accidentally transported to the golgi
acidic environment of golgi causes KDEL peptide to bind to KDEL receptor
KDEL receptor causes KKXX to recruit COPI coat proteins and form the COPI vesicle
trafficking from golgi to the lysosomes
in the golgi, there are many sugar modifying enzymes depending on sections of the Golgi
the golgi functions to modify proteins by adding or removing sugars
Golgi as a sorting station
COPI vesicles to TRANS golgi
adapter protein coated vesicles to directly go to lysosomes
can work together to send vesicles to endosome or lysosome
M6P sorting signal
GlcNAc recognizes lysosomal enzyme by specific sequences
enzyme has a mannose branch attached
GlcNAc brings lysosomal enzyme to phosphorylated sugar (enasidoglucosamine)
phosphodiesterase cleave extra sugar on the phosphate
phosphate can be recognized by M6P receptor in trans golgi to get enzyme/protein to lysosome
trans Golgi to the lysosomes process
due to slightly acidic conditions, the receptor binds to the phosphate
recuits AP and clatherin to form caltherin-coated vesicles
the coat proteins gets removed and uncoated vesicle goes to late endosome
even more acidic pH causes dissociation of mannose from receptor in the late endosome
2 more items...
lysosomal storage disease
when lysosomal enzymes are absent causing the accumulation of undegraded material
causes of inclusion cell disease
no GlcNAc
causes no M6P signal
lysosomal enzymes are secreted and not sorted
undigested glycolipids that normally degraded accumulate in lysosomes
clatherin coated proteins to promote budding to late endosome then to lysosome
secretory vesicles
constitutively sending proteins to the membrane
sending proteins to the membrane in a more regulated way
internalizing extracellular materials
phagocytosis
for large particles
pinocytosis
non selective and is for liquids
receptor-mediated endocytosis
a selective internalization of specific extracellular molecules
Low-density lipoprotein (LDL)
structure
cholesterol in apolar core
apolipoprotein wrapped around outside to guide cells to LDL receptors
phospholipid on outside
how cholesterol is transported
how it is internalized
LDL binds at 4/5 degrees to receptors
clatherin helps internalize the the LDL
the integral receptor protein and integral cargo protein receptor recruits AP1 and AP2
clatherin is recruited as well
a cage like structure is made
GTP hydrolysis causes dynamin to pinch in and form the clatherin coated vesicle
1 more item...
LDL receptor
a short c-terminal cytosolic segment with a sorting signal
1 more item...
ligand binding arm
ligand binding arm that binds to ApoB at physiological pH
1 more item...
overall internalizing process
LDL receptor binds to the ApoB protein
receptor recruits AP2 and clatherin
using GTP and dynamin the vesicle pinches off
vesicle sheds off coat proteins and fuses with late endosome
low pH causes the LDL to come off the the ligand binding arm attaches to propeller domain
importance
causes high cholesterol in blood with can clog arteries' lumen
mutations to LDLR is the cause
no LDL receptor is present
LDL receptor binds LDL poorly
LDL receptor cannot internalize the LDL
causes xanthoma (fat accumulation) and stroke at/heart attack at early age
Transferrin cycle
how iron is transferred to the circulatory system
same process as the LDL process
only difference: in late endosome, low pH causes the iron to dissociate from the ligand (ligand is still bound to receptor)
when recycled and receptor goes to neutral pH, the ligand THEN dissociates
autophagy
the degrative process in eukaryotes that degrades problematic macromolecules
pathway
degradation of misfolded proteins
Atg 8 guides lipid around misfolded protein to form isolation membrane (forms autophagosome)
other Atg proteins completes formation of double membrane and guide it to lysosome
brought to lysosome to degrade and reuse degraded parts
degradation of damaged organelles (i.e. mitochondria)
Atg 8 guides lipid around misfolded protein to form isolation membrane (forms autophagic vesicle)
experiments
Atg 5 in mice
overexpression causes longer life span
under expression causes accumulation of aggregates that causes neurodegen effects, behavioral deficits and shorter life span
Atg 8 in flies
overexpression causes longer life span due to less aggregates
under expression causes lower life span due to more aggregates