Cell Communication Flashcards
How is the speed of response modulated?
Changes in gene expression are slow
altering proteins function (turning on and off) is fast
Why is cell signaling complex?
1) Combination of signals are often needed to provoke the appropriate response
2) Multiple steps involved
3) Crosstalk bt pathways
How do small molecules differ in the signals they provoke?
Amino acids, proteins, and peptides: can’t get across membrane, need a cell surface receptor
Gas and small molecules can diffuse across membrane
How does acetylcholine act in skeletal muscles v cardiac muscles?
In skeletal muscles: acetylcholine binds to a transmembrane receptor that allows Na into the cell, Na depolarizes cell and opens organellar receptors for Ca that let Ca in and cause contraction
In cardiac cells: acetylcholine binds to a diff transmembrane receptor (trimeric G protein) that activates K+ channels and lets K+ out so hyperpolarizes the cell and the muscle relaxes
What does epinephrine do in diff cells?
Dilates bv in muscles
increase heart contraction
activates glycolysis in the liver
constricts bv in skin
Paracrine signalling
Signals from nearby cells, do not enter blood stream, speed of diffusion somewhat controlled by fluidity of ECM (extra cellular matrix)
Different concentrations can provoke different responses (eg morphogens during development)
Endocrine signalling
long distances (eg hormones), enter blood stream, receptors generally have a high affinity for the signal because have to travel far, often very dillute
Cell contact signaling
Like an axon to a target cell, very close by, so receptors have low affinity for signal molecules (which means signal can be endocytosed back into releasing cell to stop signal)
Positive Feedback
Increases signal strength, can remove signal and still get a response bc enzyme that amplifies signal now acts as that signal
Negative feedback
Can decrease signal strength, but can also oscillate signal (turn off, signal comes back, turn off, etc). therefore can alter signal strength and frequency
What is Direct Action and how does it work?
Steroids or small hydrophobic molecules diffuse across the plasma membrane and activate gene expression either by binding to TF in the cytosol and changing conformation so can go into nucleus or binding to TF directly in cytosol
TFs turn on primary response genes that make proteins that turn on secondary response genes that make the proteins that change cell behavior, primary response genes can also make proteins that turn off the 1 response genes, inhibiting the signal
How do we turn off a signal?
- degrade receptor in a lysosome
- Phosphorylate receptor and recruit masking proteins to cover cytosolic domain
- Low affinity ligans can be digested by enzymes in intracellular space or endocytosed back into releasing cell
- Decrease Ca levels by pumping Ca out of cell or into intracellular organelles
What are four signaling pathways prevalent in cells?
1) Trimeric G proteins
2) Receptor tyrosine kinases
3) Map kinases
4) CAM Kinase II
What is the mechanism of Trimeric G proteins
GTP-binding protein, GTP binds to alpha subunit (when connected to a 7 transmembrane protein), the subunits dissociate and the G alpha unit can activate other things downstream, an example being adenyl cyclase which converts AMP to cAMP, cAMP then binds to the regulator units of a PKA which can phosphorylate other things downstream
Gai subunit inhibits adenyl cyclase and Gas subunit activates it
What are the two disorders associated with improper trimeric G signaling?
1) Cholera toxin binds to the Gas subunit and keeps it from hydrolyzing GTP so its always on, this means a lot of cAMP is made which opens Cl- channels and lets Cl- leave the cell, water follows
2) Pertussis toxin binds to Gai subunit and keeps it from turning the adenyl cyclase off, so same consequence as cholera toxin, just another route
