DEFECTS IN COURTSHIP AND VISION CAUSED BY AMINO-ACID SUBSTITUTIONS INA PUTATIVE RNA-BINDING PROTEIN ENCODED BY THE NO-ON-TRANSIENT-A (NONA) GENE OF DROSOPHILA

Citation
Kg. Rendahl et al., DEFECTS IN COURTSHIP AND VISION CAUSED BY AMINO-ACID SUBSTITUTIONS INA PUTATIVE RNA-BINDING PROTEIN ENCODED BY THE NO-ON-TRANSIENT-A (NONA) GENE OF DROSOPHILA, The Journal of neuroscience, 16(4), 1996, pp. 1511-1522
Citations number
78
Categorie Soggetti
Neurosciences,Neurosciences
Journal title
ISSN journal
02706474
Volume
16
Issue
4
Year of publication
1996
Pages
1511 - 1522
Database
ISI
SICI code
0270-6474(1996)16:4<1511:DICAVC>2.0.ZU;2-Z
Abstract
The Drosophila no-on-transient A (nonA) gene is involved in the visual behaviors and courtship song of the fly. The NONA polypeptide contain s two copies of the RNA-recognition motif (RRM), a hallmark of protein s involved in RNA binding, and an adjacent conserved charged region. T his 311-amino-acid region is found in four other proteins and largely overlaps the Drosophila-Behavior/Human Splicing (or DBHS) domain. The newest family member, Drosophila nAhomo, was discovered in a database search, and encodes a protein with 80% identity to NONA. In this study , three nonA mutations generated by chemical mutagenesis were sequence d and found to fall within the conserved region. Site-directed mutagen esis of the two RRMs, and within a (conserved) charged region located C-terminal to them, was performed to determine the significance of the se domains with respect to whole-organismal phenotypes. Behavior and v iability were assessed in transformed flies, the genetic background of which lacks the nonA locus. Point mutations of amino acid 548 in the charged region confirmed the etiology of the nonA(diss) courtship-song mutation and showed that a milder substitution at this site produced intermediate singing behavior, although it failed to rescue visual def ects. Mutagenesis of the RRM1 domain resulted in effects on viability, vision, and courtship song. However, amino acid substitutions in RNP- II of RRM2 led to near-normal phenotypes, and the in vivo nonA mutatio ns located in or near RRM2 caused visual defects only. Thus, we sugges t that the first RRM could be important for all functions influenced b y nonA, whereas the second RRM may be required primarily for normal vi sion.