3.8.3.     Mutational effect

VPCs will not form a vulva if the lin-3 gene is mutated and become part of the hypodermis (skin). If the anchor cell is destroyed, the three outer cells, which normally form hypodermis, generate vulval cells instead.

In the case of lateral signalling other VPCs, P7.p becomes 1° in a lin-15 multivulva mutant in the absence of the gonad. The two cells adopt a 1°-2° or 2°-1° pattern at random If P8.p is also present. P7.p

In the case of sequential signalling, mosaic analysis of let-23.  yellow, 3° fate; red, 2° fate; blue, 1° fate. The genotype of VPCs in the key mosaic animal as follows (-/- lacking let-23 activity) (+/+let-23activity present). all VPCs become 3° in the absence of let-23. In mosaic animals which have let-23 in P6.p but lack let-23 in P5.p and P7.p show that the vulva is usually wild-type. This observation indicates for presumptive 2°VPCs, let-23(+) is not required.

The pattern of VPC cell fates direct level of LIN-3. The six VPCs adopt the 3°-3°-2°-1°-2°-3° pattern in each wild-type case. Animals with reduced lin-3 function (lin-3(rf) show lin-3 reduction of function) display that P6.p induced to 1°. A highly penetrant vulvaless phenotype resulted from a further decrease in lin-3 function. Through anchor cell excessive lin-3  (lin-3(+ + +)) results in an expansion of the pattern, means more than one central cell.

In lin-17 mutants, vulva gets the form by  P5.p and P6.p or may be posterior pseudo-vulva get from by P7.p.

Constitutive 23 mutation causes a MUltiVulva (Muv) phenotype. Typically have a single functional vulva in multivulva hermaphrodites and additional ventral protrusions vulval tissue form each pseudovulva. A psuedovulva posterior to the normal vulva resulted from a mutation within the reversed polarity of P7.p 2° lineage.

There are fewer VPC divisions in the cye-1 mutant.

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