The gene "X" codes for the membrane-associated protein X. It is a receptor used in signal transduction. When a ligand binds the receptor protein, it activates a signal transduction pathway in the cell. A mutant allele of this gene, X0, encodes a hyperactive X protein, which has the same size as the wild type and associates with the plasma membrane like the wild type, but is always active: unlike the normal protein, it activates the signal transduction pathway whether or a ligand is bound to it. Interestingly, X/X0 heterozygotes and X0/X0 homozygotes both have shorter legs and arms. With respect to the function of the X gene, the X0 allele can be considered:

(A) haploinsufficient.
(B) dominant to the Xallele.
(C) codominant to the X allele.
(D) haplosufficient.
(E) incompletely dominant to the Xallele.
(F) recessive to the X allele.

Take a look at it, from the question; the heterozygotes and the homozygotes mutants have the same phenotypes (shorter legs and arms), i.e X/XO and XO/XO have identical phenotype.

Also, the XO produces the mutant protein (encoding a hyperactive X protein), which is always active in order for the signal transduction to take place in the cells with XO protein on the plasma membrane. This same signal is developed in the transduction pathway with the second messenger in the cytosol so that both the X/XO and XO/XO will have the same phenotype. As such, we can thereby conclude that the XO allele is dominant to the X allele.