(Golic, 1994)

(Marygold et al., 2007, Leicht and Bonner, 1988)

(Golic, 1994)

(del Prado and Ripoll, 1983)

(del Prado and Ripoll, 1983)

(del Prado and Ripoll, 1983)

(del Prado and Ripoll, 1983)

The genetically defined "M(3)67C" locus (characterized by previous aneuploidy analyses) likely comprises two separable, closely linked Minute genes ("RpS9" and "RpS17").

(Marygold et al., 2007)

Source for merge of RpS17 BcDNA:RE44119 was a shared cDNA ( date:030728 ).

(FlyBase, 1996-)

Most assignments of allelism based on map positions in the vicinity of 3-30; RpS17⁴ through RpS17⁷ assigned on the basis of complementation results (del Prado, 1983; Persson, 1977).

Likely Minute gene.

(Marygold et al., 2007)

A deletion removing both RpS9 and RpS17 but no other cytoplasmic ribosomal protein-encoding genes shows Minute phenotypes.

(Marygold et al., 2007)

In a sample of 79 genes with multiple introns, 33 showed significant heterogeneity in G+C content among introns of the same gene and significant positive correspondence between the intron and the third codon position G+C content within genes. These results are consistent with selection adding against preferred codons at the start of genes.

(Kliman and Eyre-Walker, 1998)

A yeast phenotypic screen efficiently identifies conserved genes from more complex organisms and sheds light on their potential in vivo functions. Induced expression of RpS17 proteins causes aberrant cell shapes reflecting defects in cytokinesis and/or cel shape maintenance.

(Edwards et al., 1994)

Isolated using a human ribosomal protein S17 cDNA as a probe.

(Maki et al., 1989)

RpS17 has been cloned and sequenced.

(Maki et al., 1989)

Mutant alleles have the developmental delay and bristle phenotype that makes them useful as markers in clonal analysis.

(Lawrence et al., 1986)

subdivisions should accompany revised localizations.

One of a class of genes (see MIN record) that when present in one, rather than two, copies, produce a characteristic phenotype consisting of short slender bristles and delayed development. Moderate alleles have good heterozygous viability; extreme alleles very late eclosing <up>45 hr according to Ferrus (1975)</up> with poor viability, and females usually sterile. Viability further reduced in presence of su(f) alleles (Girton, Langner, Cejka, 1986).