Question

In: Biology

In the nematode C. elegans, the vulva forms from a group of six vulval precursor cells...

In the nematode C. elegans, the vulva forms from a group of six vulval precursor cells (VPCs). These cells give rise to the three vulval lineages: 1º (central vulva), 2º (lateral vulva), and 3º (hypodermis). Experiments have determined that these cells constitute an “equivalence group”, meaning that they are each capable of forming all three vulval lineages. The crucial factor in their fate decision turns out to be their proximity to the anchor cell, which is a cell located in the central region of the gonad of the developing worm:

These experiments suggest that some signal produced by the anchor cell is required to specify vulval fates. You have decided to carry out a study to identify the molecular basis for this signal. You begin by performing a genetic screen for mutants that lack a vulva (“vulvaless” mutants). One of the mutations you identify in this screen affects a gene called lin-3, which encodes a secreted protein related to the epidermal growth factor (EGF) family.

Propose a hypothesis about the possible role of lin-3 in vulval specification in the C. elegans embryo.

Solutions

Expert Solution

According to the question, the absence of lin-3 gene stops the vulva development in C.elegans. Another clue is that lin-3 is an epidermal growth factor like protein.
it is very obvious from the clues that lin-3 acts as a signalling molecule that is received by receptors on the surface of vulva precursor cells(VPC).
The anchor cells releases the growth factor i.e. Lin-3 and VPC have receptor on their surface that receives the signal.

Since , there are three possible fates for a VPC, the concentration of Lin-3 also must be responsible for the VPC fate. The cells closer to the Anchor cell must receive largest amount of VPC and thus assume primary fate and those cell farther away must assume secondary fate and tertiary fate  depending on the concentration of Lin-3.

A simple experiment where anchor cells are destroyed can be done to confirm the hypothesis. According to the hypothesis, on destroying the anchor cell, no vulva a formation will take place.

Another experiment in which some of the VPCs are destroyed can also be done. Since VPCs forms and equivalence group, destroying some of the VPC will lead to overtaking the place by remaining VPCs which will have primary, secondary and tertiary fates.

although it is not asked in the question, having an overview of vulva development in C.elegans will help understand the question better. For the same reason I am uploading a flow chart showing different signalling molecules and receptors involved in the process. For this question knowledge uptill here is also enough.


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