FlyBase Allele Report: Dmel\N[spl-1]

General Information

Symbol

Dmel\N^spl-1

Species

D. melanogaster

Name

FlyBase ID

FBal0012900

Feature type

allele

Associated gene

Dmel\N

Associated Insertion(s)

Carried in Construct

Also Known As

spl, N^spl, split, spl¹, N^sp1

Genomic Maps

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Allele class

antimorphic allele - genetic evidence

gain of function allele

hypomorphic allele - genetic evidence

Mutagen

Nature of the Allele

Allele class

antimorphic allele - genetic evidence

(de Celis and Garcia-Bellido, 1994)

gain of function allele

(Hing et al., 1999)

hypomorphic allele - genetic evidence

(Brennan et al., 1997)

Mutagen

Mutations Mapped to the Genome

Type

Location

Additional Notes

References

point mutation

X:3,164,361..3,164,361 [+]

Nucleotide change:

T3164361C

Amino acid change:

I578T | N-PA; I578T | N-PB

Reported amino acid change:

I578T

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

(Lieber et al., 1992)

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

Progenitor genotype

Cytology

Polytene chromosomes normal.

(Lindsley and Zimm, 1992)

Nature of the lesion

Statement

Reference

Amino acid replacement: I578T.

(Lieber et al., 1992)

Mutation is within EGF-like repeat 14 of the N extracellular domain.

(Lieber et al., 1992)

Substitution of an isoleucine for a threonine in EGF-repeat number 14.

(Baker et al., 1990)

A missense mutation in the extracellular EGF-like domain.

(Ramos et al., 1989)

Carried on aberration

Dp(1;1)Gr

Expression Data

Reporter Expression

Additional Information

Statement

Reference

Marker for

Reflects expression of

Reporter construct used in assay

Human Disease Associations

Disease Ontology (DO) Annotations

Models Based on Experimental Evidence ( 0 )

Disease

Evidence

References

Modifiers Based on Experimental Evidence ( 0 )

Disease

Interaction

References

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Phenotypic Data

Phenotypic Class

decreased cell number | third instar larval stage

(Cordero and Cagan, 2010)

increased cell death | somatic clone

(Li et al., 2003)

size defective | adult stage

(Cordero and Cagan, 2010)

viable

(Cagan and Ready, 1989)

visible

(Schaaf et al., 2009, Jones et al., 2006, Ramain et al., 2001, Rollins et al., 1999, Rabinow and Birchler, 1990, Cicak and Oster, 1957)

visible | dominant

(Lai et al., 1998, Campos-Ortega and Knust, 1990)

visible | dominant | neurogenic phenotype

(Brennan et al., 1997)

visible | recessive

(Indrasamy et al., 2000, Nagel and Preiss, 1999, Gorman and Girton, 1992, Lindsley and Zimm, 1992, Mari-Beffa et al., 1991, Held, 1990, Alton et al., 1989, Cagan and Ready, 1989, Ramos et al., 1989, Shepard et al., 1989, Knust et al., 1987, Shellenbarger and Mohler, 1975, Meyer, 1952, Lewis, 1945)

visible | recessive | heat sensitive

(Lindsley and Zimm, 1992, Foster, 1973)

Phenotype Manifest In

adult thoracic sensillum

(Indrasamy et al., 2000, Brennan et al., 1997)

chaeta

(Xu et al., 1990)

cone cell | third instar larval stage

(Cordero and Cagan, 2010)

dorsocentral bristle

(Nagel and Preiss, 1999)

eye

(Cordero and Cagan, 2010, Kahali et al., 2009, Schaaf et al., 2009, Jones et al., 2006, Li et al., 2003, Indrasamy et al., 2000, Hing et al., 1999, Nagel and Preiss, 1999, Rollins et al., 1999, Lindsley and Zimm, 1992, Campos-Ortega and Knust, 1990, Rabinow and Birchler, 1990, Xu et al., 1990, Cagan and Ready, 1989, Shepard et al., 1989, Shellenbarger and Mohler, 1975, Cicak and Oster, 1957, Lewis, 1945)

eye | heat sensitive

(Foster, 1973)

eye | male

(Li and Baker, 2004)

eye | somatic clone

(Li et al., 2003)

eye photoreceptor cell

(Campos-Ortega and Knust, 1990)

interommatidial bristle

(Jones et al., 2006, Lai et al., 1998)

interommatidial bristle | ectopic

(Lai et al., 1998)

macrochaeta

(Hing et al., 1999, Rollins et al., 1999, de Celis and Garcia-Bellido, 1994, Lindsley and Zimm, 1992, Rabinow and Birchler, 1990, Shellenbarger and Mohler, 1975, Cicak and Oster, 1957, Meyer, 1952)

macrochaeta | ectopic

(Shellenbarger and Mohler, 1975)

macrochaeta | heat sensitive

(Foster, 1973)

mesothoracic leg sensillum

(Held, 1990)

mesothoracic metatarsus

(Held, 1990)

mesothoracic tarsal bristle

(Held, 1990)

microchaeta

(Ramain et al., 2001, Nagel and Preiss, 1999, de Celis and Garcia-Bellido, 1994)

microchaeta | ectopic

(Shellenbarger and Mohler, 1975)

ocellar bristle

(Shellenbarger and Mohler, 1975)

ommatidial precursor cluster

(Cagan and Ready, 1989)

ommatidium

(Jones et al., 2006, Nagel and Preiss, 1999, Campos-Ortega and Knust, 1990, Shellenbarger and Mohler, 1975)

ommatidium & eye disc | male

(Li and Baker, 2004)

ommatidium | heat sensitive

(Foster, 1973)

ommatidium | somatic clone

(Li et al., 2003)

photoreceptor | third instar larval stage

(Cordero and Cagan, 2010)

photoreceptor cell & eye disc | male

(Li and Baker, 2004)

photoreceptor cell R7 | ectopic | somatic clone

(Li et al., 2003)

photoreceptor cell R8 & eye disc | male

(Li and Baker, 2004)

photoreceptor cell R8 | somatic clone

(Li et al., 2003)

presutural bristle

(Shellenbarger and Mohler, 1975)

scutellar bristle

(Kahali et al., 2009, Schaaf et al., 2009, Indrasamy et al., 2000)

scutellar bristle | ectopic

(Kahali et al., 2009)

sternopleural bristle

(Indrasamy et al., 2000)

supraalar bristle

(Shellenbarger and Mohler, 1975)

tarsal segment | heat sensitive

(Foster, 1973)

tormogen cell

(Nagel and Preiss, 1999)

vibrissae

(Indrasamy et al., 2000)

wing | heat sensitive

(Foster, 1973)

Detailed Description

Statement

Reference

The retinas of N^spl-1 third instar larvae have a reduced number of photoreceptors and cone cells compared to wild type.

The adult eyes of N^spl-1 mutants are reduced in size compared to controls.

(Cordero and Cagan, 2010)

N^spl-1/Y flies display a uniformly rough and reduced eye.

85-90% of N^spl-1/Y flies exhibit split and missing scutellar macrochaetes, whereas they display ectopic scutellar macrochaetes with attenuated (~45%) severity.

(Kahali et al., 2009)

Mutants have scutellar bristle defects (missing or twinned bristles).

(Schaaf et al., 2009)

Mutants have a reduced, rough eye with missing or double bristles.

(Jones et al., 2006)

Hemizygous N^spl-1 males have small, rough eyes. Some R8 cells and ommatidia are missing, while other ommatidia have abnormal R8 cells and lack other photoreceptor cells in N^spl-1/Y eye imaginal discs.

(Li and Baker, 2004)

When N^spl-1 clones are made in the developing eye, animals have fewer ommatidia and ommatidia with less than the normal complement of differentiated cells. Cell death is increased in mutant eyes. Many R8 precursors are absent. In about 13% of ommatidia with N^spl-1 clones ectopic R7 photoreceptor cells are seen.

(Li et al., 2003)

Mutant flies have 120.22 +/- 1.34 thoracic microchaetae per heminotum (compared to the wild-type number of 130.35 +/- 1.54).

(Ramain et al., 2001)

N^spl-1 mutants exhibit rough and small eyes.

N^spl-1 mutants exhibit elevated levels of asymmetry and reduced mean character size relative to Canton-S flies for thoracic bristles. These mutants also display significantly elevated asymmetry relative to Canton-S for scutellar, vibrissa and carnia as well as sternopleural bristles.

(Indrasamy et al., 2000)

Homozygotes show small rough eyes and split bristles.

(Hing et al., 1999)

Dorsocentral bristles appear split due to a duplication of the bristle shaft at the expense of the socket cell. Conversely, at the back of the head, double sockets appear instead of microchaetae. Homozygous females have smaller eyes of rough appearance due to irregular spacing of ommatidia.

(Nagel and Preiss, 1999)

Small rough eyes, twinned bristles and missing bristles.

(Rollins et al., 1999)

Heterozygous females have largely wild-type eyes, although missing or double interommatidial bristles are sometimes seen.

(Lai et al., 1998)

Heterozygotes have a neurogenic phenotype and have an increase in the number of thoracic bristles compared to wild-type. The number of bristles is restored almost to wild-type in N^spl-1; Dp(1;2)51b double heterozygotes.

(Brennan et al., 1997)

Eye size of N^spl-1 is increased in males that are homozygous for mle⁴.

(Hiebert and Birchler, 1994)

Macrochaetae and microchaetae lost or affected by abnormal differentiation are those that are most sensitive to Abruptex mutants. In combination with a N null allele, N^spl-1 causes extra macrochaetae and microchaetae. In presence of a N duplication, the mutant phenotype is reduced but not suppressed.

(de Celis and Garcia-Bellido, 1994)

Clones mutant for spl on the thorax display a loss of function phenotype: more bristles are formed.

(Heitzler and Simpson, 1993)

N^spl-1 heterozygotes have essentially wild-type eyes. N^spl-1 heterozygotes also carrying Egfr^E3 or Egfr^E1 have rougher eyes. Hemizygous N^spl-1 animals homozygous for Egfr^E3 or Egfr^E1 have almost no facets, the eyes being composed almost entirely of pigment cells and bristles.

(Baker and Rubin, 1992)

Individuals homozygous for Bpt¹ and N^spl-1 exhibit no Bpt¹ phenotype and an enhanced spl phenotype.

(Duus et al., 1992)

Small rough eyes and missing or doubled bristles.

(Gorman and Girton, 1992)

Eyes rough and small. Many bristles doubled, sometimes missing. Bristle effect caused by an extra division of initial bristle-forming cell (FBrf0005804). Few bristles (but not their sockets) regularly removed from posterior border of tergites in N^spl-1/+ heterozygotes (Welshons). N^64d6 N^spl-1 flies cannot be distinguished from N^64d6/+ flies. When N^spl-1 is coupled to N^64d6, N^spl-1 is not enhanced by E(spl)¹. A temperature-sensitive effect is shown by N^264-103/N^spl-1 flies, which have abnormal eye facets at 28-29^oC but are almost wild type at 20-22^oC. The spl phenotype can be enhanced by E(spl)¹/+ or E(spl)¹/E(spl)¹. N^spl-1/+;E(spl)¹/+ flies resemble N^spl-1/N^spl-1 flies; N^spl-1/N^spl-1; E(spl)¹/+ and N^spl-1/Y;E(spl)¹/+ flies show a very extreme mutant phenotype. N^spl-1/Y; gro^E73/+ males and N^spl-1/+; gro^E73/+ females show spl and Ax-like phenotypes (Xu et al.). The spl phenotype is reduced in mam heterozygotes. When, however, N^spl-1 is coupled to a N point mutant, as in N^64d6 N^spl-1/++; E(spl)¹/+, the phenotype is not spl. The N^spl-1 phenotype becomes dominant if N^spl-1 is coupled, in cis, to lethal Ax alleles. RK1.

(Lindsley and Zimm, 1992)

Phenotypes have topographic pattern specificities. Homozygotes show duplications and absence of trichogens preferentially in posterior and medial regions of the tergites.

(Mari-Beffa et al., 1991)

Increase in microchaetae density in the mesonotum when in combination with N amorph alleles and absence of macrochaetae when homozygote.

(de Celis et al., 1991)

Eye discs contain well-spaced clusters of cells with apically disposed nuclei, the number and arrangement of the cells is grossly abnormal. More than one boss-expressing cell was observed within many clusters. Prior to row 6 many cells per cluster contain boss-immunoreactive multivesicular bodies, boss is internalized as soon as boss expression is present on an adjacent cell surface. This correlates with a decrease in the number of R1-R6 neurons and an increase in the number of R7 neurons.

(van Vactor et al., 1991)

Homozygotes and hemizygotes have rough eyes which are slightly reduced in size compared to wild-type. Individual ommatidia are missing and ommatidia often contain fewer photoreceptor cells than normal and have defects in other ommatidial cell types. Photoreceptor cell axons appear normal.

(Campos-Ortega and Knust, 1990)

The total number of bristles on the basitarsi of the second legs is increased and the number of sensilla is decreased. A number of shaftless, misshapen sockets are seen.

(Held, 1990)

Homozygotes have small rough eyes due to reduced number of facets and twinned or missing bristles (FBrf0049795). Eye phenotype can be suppressed by sca and enhanced by extra copies of sca⁺ and vg⁺, the bristle phenotype is unaffected.

(Rabinow and Birchler, 1990)

Pronounced eye phenotype. Does not interact with dx^ENU.

(Xu and Artavanis-Tsakonas, 1990)

Small rough eyes and duplicated bristles.

(Xu et al., 1990)

Haploabnormal wing phenotype.

(Alton et al., 1989)

Early ommatidia in homozygous third instar discs are often poorly arranged and contain an abnormal number of cells. Rarely a single photoreceptor cell is found, and mitotic figures occasionally occur abnormally close to the furrow. By midpupation ommatidia often contain abnormal numbers of photoreceptors, cone cells and secondary pigment cells. Bristles are scattered and photoreceptors can be found beneath the retina. The eye is smaller than normal. Temperature shifts of third-instar N^l1N-ts1 larvae phenocopy the external defects of N^spl-1.

(Cagan and Ready, 1989)

Adult eyes rough, slightly reduced, with irregular facets and multiple setae. Irregular size, shape and composition of ommatidia: fewer than normal rhabdomeres per ommatidium. Eye disc pattern, shape and size irregular.

(Renfranz and Benzer, 1989)

Heterozygoutes have rough eyes. Hemizygotes show a more extreme reduction in eye size than homozygotes as well as an increase in facet and bristle abnormalities. N^spl-1/Y; E(spl)¹/+ flies show a very extreme mutant phenotype.

(Shepard et al., 1989)

Dp(2;Y)G44 males crossed to a stock carrying N^spl-1 produce sons that have straight wings or curly wings. Curly wings result from trisomy for the 44C--50B region: enhance the mutant effect of N^spl-1.

(Birchler, 1988)

The split phenotype becomes dominant if N^spl-1 is coupled, in cis, to lethal Ax alleles.

(Kelley et al., 1987)

Homozygotes and hemizygotes develop small and rough compound eyes. Some macrochaetae are split or completely missing. The presence of one copy of E(spl)¹ causes N^spl-1 to acquire a dominant phenotypic expression in all its traits. Dp(3;3)Su⁸ exerts a slight enhancing effect of the N^spl-1 phenotype.

(Knust et al., 1987)

Homozygous have small eyes with a rough, pebbly surface. Some bristles are doubled, while others, such as the ocellar, supraalar and presutural bristles are missing, and some extra hairs are present. These phenotypes are the same at 18, 25 and 29^oC.

(Shellenbarger and Mohler, 1975)

Hemizygotes and homozygotes have reduced eyes with an irregular facet arrangement, and missing or doubled bristles are frequently seen. N^264-103/N^spl-1 flies show wing nicking and tarsal segment fusion phenotypes and also show the N^spl-1 eye phenotype. The mutant eye and wing phenotypes are more strongly expressed at high temperatures than low temperatures, and tarsal fusion only occurs at high temperatures. At 20-22^oC, the eyes approach wild type but usually contain small, irregularly positioned areas of facet disarray, while at 28-29^oC the facet disarray extends over the whole surface of the eye. The temperature sensitive periods of these phenotypes occur during the third larval instar stage.

(Foster, 1973)

The split phenotype becomes dominant if N^spl-1 is coupled, in cis, to lethal Ax alleles. When N^spl-1 is coupled to a N point mutant, as in N^64d6,N^spl-1/++; E(spl)¹/+, the phenotype is not split.

(Welshons, 1971)

N^68j/N^spl-1 flies have a N^spl-1 phenotype.

(Hayman and Maddern, 1969)

N^M/N^spl-1 flies have roughened eyes which are smaller than normal and split bristles.

(Cicak and Oster, 1957)

N⁴⁷ⁱ/N^spl-1 flies have a bristle phenotype but not a roughened eye phenotype. No phenotype is seen in N^51d/N^spl-1 flies.

(Meyer, 1952)

Homozygotes have rough eyes.

(Lewis, 1945)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

N^spl-1 has visible phenotype, enhanceable by vtd^80Fh-36/vtd[+]

(Schaaf et al., 2009)

N^spl-1 has visible phenotype, enhanceable by vtd^γ26-6/vtd[+]

(Schaaf et al., 2009)

N^spl-1 has visible | dominant phenotype, enhanceable by E(spl)m8-HLH¹

(Nagel and Preiss, 1999)

E(spl)m8-HLH¹, N^spl-1 has visible | dominant phenotype, enhanceable by ato⁵

(Nagel and Preiss, 1999)

E(spl)m8-HLH¹, N^spl-1 has visible | dominant phenotype, enhanceable by ato³

(Nagel and Preiss, 1999)

E(spl)m8-HLH¹, N^spl-1 has visible | dominant phenotype, enhanceable by da⁵

(Nagel and Preiss, 1999)

E(spl)m8-HLH¹, N^spl-1 has visible | suppressible phenotype, enhanceable by sca^unspecified

(Nagel and Preiss, 1999)

N^spl-1 has visible | dominant phenotype, enhanceable by E(spl)m8-HLH^K:CAACdel

(Lai et al., 1998)

N^spl-1 has visible | dominant phenotype, enhanceable by E(spl)m8-HLH^K1K2mut

(Lai et al., 1998)

N^spl-1 has visible | dominant phenotype, enhanceable by Df(3R)Dl-FX3

(Brennan et al., 1997)

N^spl-1 has visible phenotype, enhanceable by E(spl)m8-HLH¹

(Campos-Ortega and Knust, 1990)

N^spl-1 has visible phenotype, enhanceable by E(spl)[+]/E(spl)m8-HLH¹

(Shepard et al., 1989)

NOT Enhanced by

Statement

Reference

N^spl-1 has visible | dominant phenotype, non-enhanceable by E(spl)m8-HLH^tLa

(Lai et al., 1998)

Suppressed by

Statement

Reference

N^spl-1 has size defective | adult stage phenotype, suppressible | partially by wg[+]/wg^l-17

(Cordero and Cagan, 2010)

N^spl-1 has decreased cell number | third instar larval stage phenotype, suppressible | partially by wg[+]/wg^l-17

(Cordero and Cagan, 2010)

N^spl-1 has visible phenotype, suppressible by snama^PX1/mnm[+]

(Jones et al., 2006)

N^spl-1 has visible phenotype, suppressible by l(2)rQ313[+]/snama^rQ313

(Jones et al., 2006)

N^spl-1 has visible | recessive phenotype, suppressible by Gp150[+]/Gp150^k11120b

(Li et al., 2003)

N^spl-1 has visible phenotype, suppressible by dsh^hs.PA

(Ramain et al., 2001)

N^spl-1 has visible | dominant phenotype, suppressible by wg^S107

(Brennan et al., 1997)

E(spl)[+]/E(spl)m8-HLH¹, N^spl-1 has visible phenotype, suppressible by Dl^BE21/Dl[+]

(Shepard et al., 1989)

E(spl)[+]/E(spl)m8-HLH¹, N^spl-1 has visible phenotype, suppressible by Dl^BE35/Dl[+]

(Shepard et al., 1989)

E(spl)[+]/E(spl)m8-HLH¹, N^spl-1 has visible phenotype, suppressible by Dl^BX40/Dl[+]

(Shepard et al., 1989)

E(spl)[+]/E(spl)m8-HLH¹, N^spl-1 has visible phenotype, suppressible by Dl[+]/Dl^BX41

(Shepard et al., 1989)

E(spl)[+]/E(spl)m8-HLH¹, N^spl-1 has visible phenotype, suppressible by Dl[+]/Dl^BX43

(Shepard et al., 1989)

E(spl)[+]/E(spl)m8-HLH¹, N^spl-1 has visible phenotype, suppressible by Dl^BX45/Dl[+]

(Shepard et al., 1989)

E(spl)[+]/E(spl)m8-HLH¹, N^spl-1 has visible phenotype, suppressible by Dl^BX46/Dl[+]

(Shepard et al., 1989)

E(spl)[+]/E(spl)m8-HLH¹, N^spl-1 has visible phenotype, suppressible by Dl[+]/Dl^CE21

(Shepard et al., 1989)

E(spl)[+]/E(spl)m8-HLH¹, N^spl-1 has visible phenotype, suppressible by Dl^CE23/Dl[+]

(Shepard et al., 1989)

E(spl)[+]/E(spl)m8-HLH¹, N^spl-1 has visible phenotype, suppressible by Dl^CE33/Dl[+]

(Shepard et al., 1989)

E(spl)[+]/E(spl)m8-HLH¹, N^spl-1 has visible phenotype, suppressible by Dl^CE34/Dl[+]

(Shepard et al., 1989)

E(spl)[+]/E(spl)m8-HLH¹, N^spl-1 has visible phenotype, suppressible by Dl[+]/Dl^BE23

(Shepard et al., 1989)

E(spl)[+]/E(spl)m8-HLH¹, N^spl-1 has visible phenotype, suppressible by Dl^CE37/Dl[+]

(Shepard et al., 1989)

E(spl)[+]/E(spl)m8-HLH¹, N^spl-1 has visible phenotype, suppressible by Dl[+]/Dl^CE43

(Shepard et al., 1989)

E(spl)[+]/E(spl)m8-HLH¹, N^spl-1 has visible phenotype, suppressible by Dl^BE24/Dl[+]

(Shepard et al., 1989)

E(spl)[+]/E(spl)m8-HLH¹, N^spl-1 has visible phenotype, suppressible by Dl^BE26/Dl[+]

(Shepard et al., 1989)

E(spl)[+]/E(spl)m8-HLH¹, N^spl-1 has visible phenotype, suppressible by Dl^BE32/Dl[+]

(Shepard et al., 1989)

NOT suppressed by

Statement

Reference

E(spl)[+]/E(spl)m8-HLH¹, N^spl-1 has visible phenotype, non-suppressible by Dl^HD82/Dl[+]

(Shepard et al., 1989)

Suppressor of

Statement

Reference

N⁺/N^spl-1 is a suppressor | partially of visible | heat sensitive phenotype of Dcr-2^UAS.cDa, Eogt^GD5084, Scer\GAL4^en.PU

(Müller et al., 2013)

Other

Statement

Reference

N^spl-1, sno¹ has lethal phenotype

(Lefevre and Peterson, 1972)

Phenotype Manifest In

Enhanced by

Statement

Reference

N^spl-1 has eye phenotype, enhanceable by E(spl)m8-HLH^1.UAS/Scer\GAL4^h-H10

(Kahali et al., 2009)

N^spl-1 has eye phenotype, enhanceable by vtd^80Fh-36/vtd[+]

(Schaaf et al., 2009)

N^spl-1 has scutellar bristle phenotype, enhanceable by vtd^80Fh-36/vtd[+]

(Schaaf et al., 2009)

N^spl-1 has eye phenotype, enhanceable by vtd^γ26-6/vtd[+]

(Schaaf et al., 2009)

N^spl-1 has scutellar bristle phenotype, enhanceable by vtd^γ26-6/vtd[+]

(Schaaf et al., 2009)

N^spl-1 has photoreceptor cell R8 phenotype, enhanceable by Scer\GAL4^GMR.PF/Dl^UAS.cLa/Scer\GAL4^GMR.PF

(Li et al., 2003)

N^spl-1 has eye phenotype, enhanceable by E(spl)m8-HLH¹

(Nagel and Preiss, 1999, Campos-Ortega and Knust, 1990)

N^spl-1 has ommatidium phenotype, enhanceable by E(spl)m8-HLH¹

(Nagel and Preiss, 1999, Campos-Ortega and Knust, 1990)

N^spl-1 has eye phenotype, enhanceable by E(spl)m8-HLH^1.UAS/Scer\GAL4^h-1J3

(Nagel et al., 1999)

N^spl-1 has eye phenotype, enhanceable by E(spl)m8-HLH::E(spl)mδ-HLH^cNa

(Nagel et al., 1999)

N^spl-1 has eye phenotype, enhanceable by E(spl)m8-HLH::E(spl)m5-HLH^E(spl).PN

(Nagel et al., 1999)

N^spl-1 has eye phenotype, enhanceable by E(spl)m8-HLH^+t2.8

(Nagel et al., 1999)

N^spl-1 has eye phenotype, enhanceable by E(spl)m8-HLH^1.tNa

(Nagel et al., 1999)

N^spl-1 has eye phenotype, enhanceable by E(spl)m7-HLH^+t5.6

(Nagel et al., 1999)

N^spl-1 has phenotype, enhanceable by Df(2R)Nipped-D263.3

(Rollins et al., 1999)

N^spl-1 has phenotype, enhanceable by Df(2R)Nipped-E43

(Rollins et al., 1999)

N^spl-1 has macrochaeta phenotype, enhanceable by Df(2R)Nipped-D341.1

(Rollins et al., 1999)

N^spl-1 has macrochaeta phenotype, enhanceable by Df(2R)Nipped-E338

(Rollins et al., 1999)

N^spl-1 has interommatidial bristle | ectopic phenotype, enhanceable by E(spl)m8-HLH^K:CAACdel

(Lai et al., 1998)

N^spl-1 has ommatidium phenotype, enhanceable by E(spl)m8-HLH^K:CAACdel

(Lai et al., 1998)

N^spl-1 has interommatidial bristle | ectopic phenotype, enhanceable by E(spl)m8-HLH^K1K2mut

(Lai et al., 1998)

N^spl-1 has ommatidium phenotype, enhanceable by E(spl)m8-HLH^K1K2mut

(Lai et al., 1998)

N^spl-1 has adult thoracic sensillum phenotype, enhanceable by Df(3R)Dl-FX3

(Brennan et al., 1997)

N^spl-1 has phenotype, enhanceable by E(spl)m8-HLH^1.tKa

(Tietze et al., 1993)

N^spl-1 has phenotype, enhanceable by rn[+]/rn^roe-KE17