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28 Cards in this Set

  • Front
  • Back
What are the things that are different in cells? (3)
-protein expression;

Genome is the same in all cells, except immune cells- no nucleus
What is combinatorial control?
Most genes are controlled by a specific combination of regulatory factors that promote and repress gene expression
Chromatin accessibility
The state of chromatins that impacts transcription factor binding to DNA and transcriptional specificity. Differences in this diversifies cells
Cell Fate
The differentiated cell type the cell will become. As cells divide, they become less totipotent and cell fate is progressively restricted. Patterns of gene expression changes, signal receptors change, so the cell can only respond to certain signals. This is regulated by transcriptional control.
Housekeeping gene
A gene expressed in every cell- used as a control to compare to genes that only specific cells express
What are the two ways to transition between cell states?
(1) extrinsic cues- cell signals;
(2) intrinsic cues- segregation of determinants- determinants go to one side of the cell so when the cell divides only one daughter cell has determinant
What do morphogens do?
Morphogens are cell signals that cells react to based on where they are in the morphogen gradient. Can cause cells to differentiate into different cell types based on how much of the morphogen is present.
Morphogens in the neural tube
Shh and BMP are neural morphogens in opposing gradients which induce expression of specific transcription factors to pattern motor neuron subtype in the developing neural tube.
Lateral Inhibition
Type of cell-cell signaling; both cells initially have the same amount of X (stable state 1), until one expresses a little more, then there's positive feedback where the cell with more gets signals to produce more and the cell with less gets signals to pr
Type of cell-cell signaling; both cells initially have the same amount of X (stable state 1) and have equal potential of becoming one type of cell or another type of cell, until one randomly expresses a little more, then there's positive feedback where the cell with more gets signals to produce more and the cell with less gets signals to produce less until there is one cell with all of X and another with none (stable state 2)
Lateral inhibition in C. Elegans
Cells Z1.ppp & Z4.aaa can make AC or VU type cells, wild type always has one of each. They're always neighbors. Killing either one of them with laser causes the other one become AC, AC is default. lin-12 null mutants- both cells AC. lin-12 gain of function or lag-2 null mutants- both cells VU. lag-2 (delta) required for VU; lin-12(notch) required for AC
What is a determinant?
A factor that is both necessary and sufficient to specify a particular cell fate
What must occur for cell division to be asymmetric? (2)
(1) Cytoplasmic or membrane components must be localized to (or enriched in) one side of the cell
(2) The mitotic spindle must be oriented such that the localized components are preferentially segregated to one daughter cell over the other
Advantages of using nematode C. elegans for developmental bio studies
Short life cycle, simple anatomy, transparent at all stages, fully defined cell lineage, conserved developmental pathways, genetically tractable
How is embryonic asymmetry generated?
C elegans embryo division & determinant
P0 parent cell divides into P1 (posterior side) and AB (anterior side). PIE-1 is a determinant that specifies the P1 line of cells, and if there is any PIE-1 left in AB, it gets degraded.
What controls asymmetric cell division? How was this discovered?
par family; par mutants only have symmetrical cell division. Different par proteins localize in different areas of the cell by reciprocal inhibition to define two different domains for asymmetric cell division
PAR family; PAR mutants only have symmetrical cell division. Different PAR proteins localize in different areas of the cell by reciprocal inhibition to define two different domains for asymmetric cell division. This was discovered by using a genetic approach by creating mutants and looking for ones where the asymmetry is lost.
What provides the initial symmetry-breaking cue?
The site of sperm entry defines posterior side-- it stops cortical streaming on that side of the cell.
What is the pathway that initiates/stops cortical actin contractility (cortical streaming)?
cortical streaming helps push PAR-3, PAR-6 to the anterior side and set up cell assymetry. To make cell streaming direction, it is shut off at the posterior side. This happens by regulating Rho-1 spacially.
What generates the force that moves the spindle?
Microtubules, because when you break the mitotic spindle with a laser, the nuclei are pushed farther away from each other because there's no force holding them together.
Why is there a greater pulling force on the posterior side?
There are more dynein complexes on the posterior side which pull the microtubules attached the nucleus closer compared to the anterior side.
What are the mechanisms for the segregation of determinants? (3)
(1) Protein segregation
(2) Differential protein stability
(3) mRNA segregation
Drosophila sensory organ development
pI is the SOP (sensory organ precursor cell) which divides asymmetrically into pIIa and pIIb. pIIa gives rise to external components, pIIb gives rise to internal components
What does Notch signaling do?
High notch signals to pIIa, and low notch signaling to pIIb. Hyperactive notch signaling transforms pIIb to pIIa. This is not lateral inhibition because numb in pIIb forces it to have low notch.
What does numb do?
It's a determinant for pIIb fate; mutants deficient of numb only have pIIa, numb overexpression leads to 2 pIIb daughter cells. Numb asymmetry depends on Par3/Par6. Numb also downregulates Notch signaling by degrading Spdo (notch cofactor).
2 approaches for identifying determinants
(1) Molecular/cellular approach- look for a factor that can trigger differentiation of precursor cells in vitro
(2) Genetic approach: look for mutants that fail to make a particular cell type
How was MyoD identified?
Using a molecular approach. Fibroblasts, which don't usually make muscle cells, treated with 5-azacC turned into myotubes. mRNA was isolated from myotubes, total cDNA was prepared, then split up and transfected into fibroblasts, and some became myotubes. Therefore, myoD is sufficient to transform fibroblasts into myotubes. MyoD is a basic-helix-loop-helix transcription factor that transcribes muscle specific genes
Is myoD necessary for muscle cell development?
No, MyoD knockout mice still had muscles. Turns out there is a family: MyoD, MyoG, Myf5,Mrf4, which are determinants for muscle cells as a family. If all are knocked out. If just one is knocked out, there are still muscles because others can make muscles.
What is the determinant for eye development?
Eyeless (in drosphila); Pax6 in mammals. It encodes a paired-HD family transcription factor. It's necessary for eye development because eyeless mutant has no eyes. Eyeless expression is sufficient because when expressed on the leg of a fly, eye begins to form there. This is a genetic approach for finding a determinant