The fruitless ( @entity15323 ) gene functions in @entity238 males to establish the potential for male @entity146 . @entity15323 encodes a complex set of sex-specific and sex-nonspecific mRNAs through the use of multiple promoters and alternative pre-mRNA processing. The male-specific transcripts produced from the distal (P1) @entity15323 promoter are believed to be responsible for its role in specifying @entity146 and are only expressed in a small fraction of central nervous system (CNS) cells. To understand the molecular etiology of fruitless mutant phenotypes, we compared wild-type and mutant transcription patterns. These experiments revealed that the @entity15323 (2), @entity15323 (3), @entity15323 (4), and @entity15323 (sat) mutations, which are due to P-element inserts, alter the pattern of sex-specific and sex-nonspecific @entity15323 RNAs. These changes arise in part from the P-element insertions containing splice acceptor sites that create alternative processing pathways. In situ hybridization revealed no alterations in the locations of cells expressing the P1- @entity15323 -promoter-derived transcripts in @entity15323 (2), @entity15323 (3), @entity15323 (4), and @entity15323 (sat) pharate adults. For the @entity15323 (1) mutant (which is due to an inversion breakpoint near the P1 promoter), Northern analyses revealed no significant changes in @entity15323 transcript patterns. However, in situ hybridization revealed anomalies in the level and distribution of P1-derived transcripts: in @entity15323 (1) males, fewer P1-expressing neurons are found in regions of the dorsal lateral protocerebrum and abdominal ganglion compared to wild-type males. In other regions of the CNS, expression of these transcripts appears normal in @entity15323 (1) males. The loss of fruitless expression in these regions likely accounts for the striking @entity854 exhibited by @entity15323 (1) males. Thus, we suggest that the mutant phenotypes in @entity15323 (2), @entity15323 (3), @entity15323 (4), and @entity15323 (sat) animals are due to a failure to appropriately splice P1 transcripts, whereas the mutant phenotype of @entity15323 (1) animals is due to the reduction or absence of P1 transcripts within specific regions of the CNS.

Aberrant splicing and altered spatial expression patterns in fruitless mutants of XXXX .

@entity854 :: ('MESH:D018376', 'Disease') :: ['courtship abnormalities'] @entity146 :: ('MESH:D001523', 'Disease') :: ['sexual behaviors', 'sexual behavior'] @entity238 :: ('7227', 'Species') :: ['Drosophila'] @entity15323 :: ('42226(Tax:7227)', 'Gene') :: ['fru']
@entity238 :: (7227,Species) :: ['Drosophila melanogaster']
