Developmental Biology Flashcards
1
Q
Techniques for analysing development
A
- Description
- Cellular description = direct observation of living embryos, needs transparency - Physical manipulation
- Removal of cells/tissues like cell isolation - Genetics/molecular experiment
- Forward genetics
- Reverse genetics
- Temp sensitive/epistasis
2
Q
Developmental principles
A
- Development occurs by epigenesis
- Development starts with a single cell
- Progressive restriction in developmental potential
- Proliferation vs cell death
- Oriented + asymmetric cell divisions
- Epithelial sheets importance
- Developmental induction
- Developmental fields
- Boundaries (fields result in boundaries)
- Signalling between cells
- Choice of fate
- Morphogenesis and cell affinities
3
Q
Benefits of using C elegans
A
- Simple but has all major cell types
- Easy to grow
- Transparent
- Different anatomy for XX vs XO
- Genetic analysis can be used to study development
- Vulva formation is a good example of tissue remodelling
4
Q
Steps in vulval development
A
- Generating VPCs (3 fates 1o,2o,3o
- Vulval precuror patterning (in L3, signal from the gonad specifies 3 VPCs to generate vulval cells, typically 3-3-2-1-2-3)
- Generation of adult cells (can be VulA-F)
- Anchor cell invasion (forms hole in epidermis)
- Morphogenesis (forms 7 distinct toroids)
5
Q
Generating VPCs
A
- 11pnp cells are formed during L1 Laval stage
- How gene lin-39 = major determinant of VPC group + is expressed in p3p-p8p
6
Q
VPC 1o, 2o and 3o pattern formation
A
- 2 systems cooperate :
1. graded signal of Lin-3 acting via Let-23
2. sequential signal of DSL ligand acting via LIN-12
7
Q
Anchor cell
A
- Ablation prior to L3 stage completely blocks vulval development
- AC produce Lin-3, whose action is graded
- Vulvaless/multivulvaless mutations
- Lin3-let23-sem5-let60-lin45-lin-1
- Signalling terminates with modulation of TF like lin-1 that controls morphogenesis
- Lin-31/lin-1 ETS complex are phosph. by MAPK → no inhibition of vulva
- P6p receives most Lin-3, , p3p + p8p have negligible
8
Q
Lateral inhibition
A
- Stops adjacent cells also adopting primary fate
- ## Genes involved in lin-12 activation are unregulated by Ras in p6p, lead to activation of lin-12/notch in p5p/p7p, helping p5p/p7p adopt 2o fate
9
Q
Negative regulation of induction
A
- 3 classes of SynMuv gene
- Need mutation in 1 class A + 1 class B
- Prevents wrong LIN-3 expression
10
Q
Formation of axes
A
- asymmetric divisions establish 3 major axes
- 5 asymmetric divisions produce 6 founder cells: AB, MS, E, C, D, P4
11
Q
Establishing A/P axis
A
- Breaking symmetry (sperm assembles PCM, CYK-4, 1st cleavage → Ab1 + P1)
- PAR proteins (PAR 3+6 form complex w/ PKC-3, needs cdc-42 to maintain polarity, PAR1+2 localise in posterior cortex)
- P granules (form germline, start in cytoplasm, move to posterior of cell)
12
Q
Spindle positioning
A
- Heterotrimeric G protein acts ds of PAR to transduce polarity
- GOA-1 + GPA-16
- GRP1/2
Dynein
13
Q
Formation of D/V axis
A
- 1st division → big AB, smaller P
- AB = symmetrical division, controlled by PAR
- P1 = asymmetric division, spindle oriented on AP axis
- 2nd division → ABa, Abp, P2 + EMS
- D + V axis different (only AB daughter cell has GLP-1 receptor, P2 has APX-1)
14
Q
Formation of L/R axis
A
- Determined by division of ABa/ABp
- LH daughter are ↑ anterior to RH, causes cell to contract
- EMS divides 1st to make E + MS
- Then P2 divides to make C + P3 which divide again to make D + P4
15
Q
Breaking symmetry
A
- All cells have same developmental potential
- However end point = differentiation
