. 2001 Jan 15;21(2):513–526. doi: 10.1523/JNEUROSCI.21-02-00513.2001

Table 1.

Lack of male-specific FRU^M protein in severely affected fruitless mutants

Genotype	Relative FRU^M immunostaining, % (n pupal CNS specimens)
WT	100 (10)
fru³/fru³	0 (6)
fru^w12/fru³	0 (3)
Df-fru^w24/fru³	0 (5)
fru^w27/fru³	0 (5)
fru³/Df-Cha^M5	0 (7)
fru^w12/Df-Cha^M5	0 (7)
fru^w27/Df-Cha^M5	0 (5)
fru^w12/Df-fru^w24	0 (3)
fru^w12/fru^w27	0 (3)
Df-fru^w24/fru^w27	0 (3)
Df-Cha^M5/Df-sat¹⁵	0 (5)
Df-fru^4-40/Df-sat¹⁵	0 (5)

Immunohistochemistry using anti-FRU^M was performed to assess expression of the male forms of FRU protein in the CNSs of 2-d-old male pupae from a wild-type (WT) stock, afru³-bearing strain, and pupal progeny resulting from crosses of fru-breakpoint variants to each other or certain such variants to fru³ (the only homozygous-viable mutant used here). The w-including genotypes are chromosome aberrations, each involving a breakpoint within the fru locus; most of the Df-including genotypes are deletions, each of which has one breakpoint at this locus and thus is missing part of the locus (Df-fru^w24removes the entire locus). Nearly all breakpoint combinations, with respect to the chromosome aberrations depicted in Figure 1, were generated, except forfru^w24/Df-Cha^M5 (which die as embryos). For the results column, the wild-type staining level was simply set at 100, because there was no apparent FRU^Mimmunostaining in pupae carrying any of these mutant orfru-breakpoint variant specimens.