C. elegans Vulval development

Question 1

How is opening and closing of vulva controlled?

Answer 1

muscles (stacked, uterine + 4 more)

neurons (VC4/5/6 + HSN, on both sides)

Question 2

At which stage of development do vulva cells arise?

Answer 2

postembryonic, L3

Question 3

Which are the 5 steps of vulval development?

Answer 3

1: generation of precursor cells (P3.p - P8.p)
2: vulval precursor patterning (1 - 3° fate)
3: generation of adult cells
4: anchor cell invasion
5: morphogenesis of the vulva

Question 4

Which VCP adopts 1° fate?

What do its descendants form?

Answer 4

P6.p

the vulva

Question 5

Which VCPs adopt 2° fate?

What do their descendants form?

Answer 5

P5.p and P7.p

the vulva

Question 6

Which VCPs adopt 3° fate?

What do their descendants form?

Answer 6

P3.p, P4.p, P8.p

descendants fuse with the hypodermis

Question 7

How did they study the role of individual cells in vulval development?

Answer 7

by ablating them with laser (shooting the cells, nucleus boils, cell dies)
if vulva did not form, they observed the Egl phenotype

Question 8

Why is timing of ablations important?

Answer 8

if cells have not acquired their cell fates yet (before 1st division), they are still multipotential and can respond to new cell environment by switching their fates

but after 1st division, they are locked in specific fate

Question 9

What is vulval equivalence group?

Answer 9

P3.p - P8.p
are multipotential (but not their descendants)

Question 10

Which cell induces the vulva/is required for VPC patterning?

Which cells does it influence?

Answer 10

anchor cell
(no vulva, if ablated)

induces P5.p - P7.p to adopt 2/1/2° fate

Question 11

What is the ground state of VPCs?

Answer 11

3° fate

Question 12

Which 3 signals play a role in VPC patterning?

Answer 12

signal 1: inductive signal
signal 2: lateral signal
signal 3: represses vulval fate of neighboring non-VPC cells

Question 13

Which models were proposed for VPC pattern formation?

Answer 13

graded anchor cell signal
adjacent cell interaction
partially graded AC signal
ungraded AC signal

Question 14

Which models are true for VPC pattern formation?

Answer 14

graded anchor cell signal
(AC signal is graded so that cell within a certain distance from AC adopts a 1° fate, slightly further away 2°, distant 3°)
adjacent cell interaction
(AC signals directly underneath -> 1° fate of P6.p; P6.p then signals adjacent cells to become 2°)

combination of those two (signal 1 + 2)

Question 15

Which are the vulva related mutant phenotypes?

Answer 15

Muv = multivulval = too much vulval induction
Vul = vulvaless (bag of worms) = not enough vulval induction

Question 16

What is the molecular nature of the inductive singal?

Answer 16

LIN-3
ligand for Ras/MAPK pathway, which is required for acquiring 1° fate
expressen in AC only

Question 17

What is signal 2 in VPC patterning?

Answer 17

lateral inhibition by LIN-12
P6.p downregulates Ras/MAPK pathway in P5.p and P7.p
(the 1st 1° cell inhibits others from becoming 1° too)

Question 18

Describe LIN-12 signaling.

Answer 18

cell that aquired 1° fate has the strongest signaling via lin-23 receptor
this leads to transcriptional upregulation of DSL ligands (Notch-like) and downregulation of lin-12 (Notch-like receptor)
DSL ligands act on LIN-12 receptor on neighboring cells and inhibit their let-23 signaling = inhibiting 1° fate

Question 19

What is signal 3 and where is it active?

Answer 19

signal 3 is inhibition of VPC fate in hyp7 cells (epidermis next to it)

inhibition by SynMuv genes class A and B (e.g. lin-8/9/35)
called synthetic because only duble KO shows phenotype (redundancy)

Question 20

Which method was used to determine where SynMuv genes are active?

Answer 20

mosaic analysis

putting genes under control of tissue specific promoters

Question 21

In step 3, which signal is needed for establishing correct P7.p polarity?

Answer 21

Wnt

Question 22

What is studying how anchor cell invades the basal lamina important for human diseases?

Answer 22

shares properties with metastatic cancer