FlyBase Allele Report: Dmel\dl[1]

General Information

Symbol

Dmel\dl¹

Species

D. melanogaster

Name

FlyBase ID

FBal0002643

Feature type

allele

Associated gene

Dmel\dl

Associated Insertion(s)

Carried in Construct

Key Links

Allele class

loss of function allele

amorphic allele - genetic evidence

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

amorphic allele - genetic evidence

(Holley et al., 1995, Lemaitre et al., 1995, Govind et al., 1993, Isoda et al., 1992, Ray et al., 1991)

loss of function allele

(Matova and Anderson, 2006, Morize et al., 1998, Bergmann et al., 1996, Huang et al., 1993)

Mutagen

ethyl methanesulfonate

(Tearle and Nusslein-Volhard, 1987, Simpson, 1983)

Mutations Mapped to the Genome

Type

Location

Additional Notes

References

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

Progenitor genotype

Cytology

Nature of the lesion

Statement

Reference

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 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

Phenotype Manifest In

amnioproctodeal invagination

(Stein et al., 1998)

cephalopharyngeal skeleton | maternal effect

(Jia et al., 2002)

denticle

(Stein et al., 1998)

embryonic/first instar larval cuticle

(Jazwinska et al., 1999, Briggs et al., 1998)

embryonic/first instar larval cuticle | maternal effect

(Jia et al., 2002)

embryonic/first instar larval cuticle | ventral

(Schupbach and Wieschaus, 1989)

embryonic/larval cuticle | maternal effect

(Ratnaparkhi et al., 2008)

embryonic epidermis | maternal effect

(Ratnaparkhi et al., 2006)

embryonic primordium of adult salivary gland

(Panzer et al., 1992)

endoderm

(Tepass and Hartenstein, 1994)

filzkorper

(Stein et al., 1998)

filzkorper | maternal effect

(Jia et al., 2002)

macrochaeta | ectopic | cold sensitive (with dl⁴)

(Ayyar et al., 2007)

mesothoracic tergum | cold sensitive (with dl⁴)

(Ayyar et al., 2007)

ventral furrow

(Stein et al., 1998)

visceral mesoderm

(Tepass and Hartenstein, 1994)

Detailed Description

Statement

Reference

VA1d olfactory receptor neuron axon targeting is normal in mutant flies.

(Ward et al., 2015)

At 29[o]C, only 47% of embryos derived from heterozygous females hatch, while the remaining embryos show slight dorsalisation.

(Gueguen et al., 2013)

At 29[o]C, about half of the dead embryos produced by dl¹/+ females exhibit detectable D/V patterning defects. The majority of embryos appear moderately dorsalised, exhibiting mildly expanded ventral denticle belts and a twisted germ band.

(Ratnaparkhi et al., 2008)

dl¹/dl⁴ flies show one ectopic macrochaeta in 39% of heminota analysed at 18[o]C (this phenotype is not seen at 25[o]C).

(Ayyar et al., 2007)

Embryos derived from homozygous females are completely dorsalised, developing into hollow tubes of dorsal epidermis.

(Ratnaparkhi et al., 2006)

The mean circulating hemocyte number of dl¹/Df(2L)TW119 mutants is not statistically different from that of controls.

(Chiu et al., 2005)

The mean ln (natural logarithm) circulating hemocyte concentration (CHC) value of hemizygous larvae is significantly higher than that of control siblings.

(Sorrentino et al., 2004)

The cuticles of embryos laid by homozygous females

lack ventral denticle belts, Filzkorper and a head skeleton and instead consist only of a tube of dorsal epidermis.

(Jia et al., 2002)

Embryos derived from dl¹ cact⁷ mothers carrying either dl^+mWT, dl^S70A, dl^S79A, dl^S103A or dl^S213A are strongly ventralised and do not hatch. Embryos derived from dl¹ cact⁷ mothers carrying dl^S312A are severely dorsalised. Embryos derived from dl¹ cact⁷ mothers carrying dl^S317A are lateralised.

(Drier et al., 1999)

The cuticle of homozygous dpp^H46 embryos consists only of ventral epidermis. This phenotype is not altered if the embryos are derived from homozygous dl¹ females. Injection of brk^cJa mRNA into dorsalised embryos derived from dl¹ females results in the development of cuticle with ventral denticles at the site of injection.

(Jazwinska et al., 1999)

Homozygous females produce embryos that differentiate apolar tubes of cuticle of the type normally found on the dorsal side of wild-type embryos. This phenotype is rescued if the females carry dl^bcd.PB - these females produce hatching larvae that have normal dorsal-ventral pattern elements.

(Briggs et al., 1998)

Embryos derived from homozygous females lack denticles and Filzkorper. Embryos derived from homozygous females show abnormal gastrulation; they do not form the ventral furrow or the posterior midgut invagination, and symmetrical "dorsal" folds develop all around the circumference of the embryo.

(Stein et al., 1998)

Single cells from N^55e11 embryos transplanted into the ventral neurogenic region of host embryos derived from dl¹ mothers give rise to neural cells in 91% of cases.

(Stüttem and Campos-Ortega, 1997)

cact⁷ dl¹ double mutants also exhibit melanotic tumours.

(Govind, 1996)

Bacterially challenged mutants exhibit a wild type Drs response. Pattern of response of CecA1 and CecA2 parallels that of Drs. Dpt and Dro remain fully inducible and pattern of expression of AttA and Def in intermediate. Infection of Tl^r3/Tl^rv1 mutants with A.fumigatus or E.coli causes survival rates similar to wild type.

(Lemaitre et al., 1996)

Embryos differentiate a cuticle comprised of only the most dorsal pattern elements. Dorsal injection of sog mRNA into dl¹ embryos causes differentiation of dorsolaterally derived structures not present in dl¹ embryos and injection of 7-fold higher sog mRNA causes differentiation of a ring of filzkorper around the embryonic circumference. Dorsal injection of sog::Xlae\chordin mRNA into dl¹ embryos causes differentiation of filzkorper.

(Holley et al., 1995)

Injection of the pll::tor^t4021p construct and tor::tub^t4021t construct into dl¹/Df(2L)TW119 and dl¹²/Df(2L)TW119 heterozygotes cannot induce dorsoventral pattern elements.

(Großhans et al., 1994)

Heterozygous twi¹ embryos from heterozygous dl¹ mothers lack various amounts of mesoderm in a temperature-dependent manner. Gaps in the visceral mesoderm are correlated with gaps in the overlying midgut epithelium.

(Tepass and Hartenstein, 1994)

Nonmotile germ cells and defective in gonad assembly when in double mutant combination with tor.

(Warrior, 1994)

In trans to cact gain of function alleles, this allele results in dorsalized embryos.

(Govind et al., 1993)

Salivary placodes are strongly reduced or completely absent.

(Panzer et al., 1992)

The tll stripe extends around the complete circumference of the embryo.

(Pignoni et al., 1992)

Dorsalized phenotype facilitates removal of perivitelline fluid.

(Stein and Nusslein-Volhard, 1992)

Interacts with RpII140^wimp maternal effect.

(Parkhurst and Ish-Horowicz, 1991)

Some cells behave as amnioserosa cells, these cells are expressed in the region of the embryo predicted by the refined expression pattern of zen.

(Ray et al., 1991)

Embryos derived from dl¹ mothers produce only the dorsal most cuticle elements.

(Schupbach and Wieschaus, 1989)

Homozygous females lay eggs differentiating to an essentially hollow epidermal tube. No organs are built besides the posterior midgut and a small group of nerve cells.

(Leiss et al., 1988)

Gastrulation in embryos derived from homozygous females is abnormal, with the transverse folds encircling the dorsalised embryo.

(Carroll et al., 1987)

dpp^Hin embryos derived from dl¹ mothers have a dorsalizing phenotype: dorsal setae covering the entire body, rudimentary posterior spiracles lacking Filzkorper and numerous ventral like setae. Individuals have an elongated and convoluted appearance.

(Irish and Gelbart, 1987)

Homozygous females produce dorsalised embryos.

(Schupbach and Wieschaus, 1986)

The presence of the N^55e11 did not affect the epidermal pattern in the thoracic and abdominal segments of hemizygotes derived from dl¹/dl¹ hemizygotes. The presence of ovo^D1 also has no effect on the dl¹ phenotype.

(Campos-Ortega, 1983)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

dl¹ has majority die during embryonic stage | dominant | maternal effect | heat sensitive phenotype, enhanceable by CsIV\I2vank3^UAS.Tag:FLAG/Zzzz\I2vank3^{Scer\UAS.T:Zzzz\FLAG}/Scer\GAL4^{VP16.mat.αTub67C}

(Gueguen et al., 2013)

dl¹ has partially lethal - majority die | dominant | maternal effect | heat sensitive phenotype, enhanceable by CsIV\Pvank1^UAS.Tag:FLAG/Scer\GAL4^{VP16.mat.αTub67C}/Zzzz\Pvank1^{Scer\UAS.T:Zzzz\FLAG}

(Gueguen et al., 2013)

dl¹ has abnormal dorsal/ventral axis specification | dominant | maternal effect | embryonic stage | heat sensitive phenotype, enhanceable by CsIV\Pvank1^UAS.Tag:FLAG/Scer\GAL4^{VP16.mat.αTub67C}/Zzzz\Pvank1^{Scer\UAS.T:Zzzz\FLAG}

(Gueguen et al., 2013)

dl¹ has majority die during embryonic stage | dominant | maternal effect | heat sensitive phenotype, enhanceable by CsIV\Pvank1^UAS.Tag:FLAG/Scer\GAL4^{VP16.mat.αTub67C}/Zzzz\Pvank1^{Scer\UAS.T:Zzzz\FLAG}

(Gueguen et al., 2013)

dl¹ has partially lethal - majority die | dominant | maternal effect | heat sensitive phenotype, enhanceable by CsIV\I2vank3^UAS.Tag:FLAG/Zzzz\I2vank3^{Scer\UAS.T:Zzzz\FLAG}/Scer\GAL4^{VP16.mat.αTub67C}

(Gueguen et al., 2013)

dl¹ has abnormal dorsal/ventral axis specification | dominant | maternal effect | embryonic stage | heat sensitive phenotype, enhanceable by CsIV\I2vank3^UAS.Tag:FLAG/Zzzz\I2vank3^{Scer\UAS.T:Zzzz\FLAG}/Scer\GAL4^{VP16.mat.αTub67C}

(Gueguen et al., 2013)

Suppressed by

Statement

Reference

dl¹ has lethal | larval stage phenotype, suppressible by Scer\GAL4^hs.PB/Dif^UAS.cIa/Dif¹

(Matova and Anderson, 2006)

Enhancer of

Statement

Reference

BacA\p35^GMR.PH, Scer\GAL4^He.PZ, dl¹ is an enhancer of increased cell number phenotype of Dif¹

(Matova and Anderson, 2006)

NOT Enhancer of

Statement

Reference

dl¹ is a non-enhancer of lethal | maternal effect | embryonic stage phenotype of Gug^unspecified

(Zhang et al., 2002)

Suppressor of

Statement

Reference

Scer\GAL4^e33C, dl^UASp.cMa, dl¹ is a suppressor of lethal | larval stage phenotype of Dif¹

(Matova and Anderson, 2006)

dl^UASp.cMa, Scer\GAL4^He.PZ, dl¹ is a suppressor of lethal | larval stage phenotype of Dif¹

(Matova and Anderson, 2006)

dl^UASp.cMa, dl¹, Scer\GAL4^hs.PB is a suppressor of lethal | larval stage phenotype of Dif¹

(Matova and Anderson, 2006)

Df(2L)J4/dl¹ is a suppressor | partially of melanotic mass phenotype | larval stage phenotype of lwr⁵/lwr^4-3

(Chiu et al., 2005)

dl⁴/dl¹ is a suppressor of abnormal immune response phenotype of wntD^KO1

(Gordon et al., 2005)

Df(2L)J4/dl¹ is a suppressor of increased cell number | larval stage phenotype of lwr⁵/lwr^4-3

(Huang et al., 2005)

NOT Suppressor of

Statement

Reference

dl¹ is a non-suppressor of abnormal neuroanatomy phenotype of Ank2^f02001

(Keller et al., 2011)

dl¹ is a non-suppressor of partially lethal - majority die | recessive phenotype of cact⁷

(Qiu et al., 1998)

Other

Statement

Reference

Dif¹, dl¹ has decreased cell number phenotype

(Matova and Anderson, 2006)

Dif¹, dl¹ has increased cell death phenotype

(Matova and Anderson, 2006)

Dif¹, dl¹ has abnormal cell size phenotype

(Matova and Anderson, 2006)

Rel^E20, dl¹ has decreased body size phenotype

(Matova and Anderson, 2006)

Rel^E20, dl¹ has partially lethal - majority die | larval stage phenotype

(Matova and Anderson, 2006)

Dif¹, dl¹ has decreased body size phenotype

(Matova and Anderson, 2006)

Dif¹, dl¹ has lethal | larval stage phenotype

(Matova and Anderson, 2006)

Dif¹, dl¹ has abnormal immune response phenotype

(Matova and Anderson, 2006)

dl¹, twi¹/twi[+] has lethal phenotype

(Wrischnik et al., 2003)

dl¹, twi¹/twi[+] has lethal | dominant phenotype

(Wrischnik et al., 2003)

dl[+]/dl¹, twi¹ has lethal phenotype

(Wrischnik et al., 2003)

dl[+]/dl¹, twi¹ has lethal | dominant phenotype

(Wrischnik et al., 2003)

Phenotype Manifest In

Enhanced by

Statement

Reference

dl¹ has embryonic/larval cuticle | maternal effect phenotype, enhanceable | maternal effect by Dlip3¹

(Ratnaparkhi et al., 2008)

Suppressed by

Statement

Reference

dl¹ has embryonic/first instar larval cuticle phenotype, suppressible by Dif^bcd.PS

(Stein et al., 1998)

dl¹ has amnioproctodeal invagination phenotype, suppressible by Dif^bcd.PS

(Stein et al., 1998)

dl¹ has denticle phenotype, suppressible by Dif^bcd.PS

(Stein et al., 1998)

dl¹ has filzkorper phenotype, suppressible by Dif^bcd.PS

(Stein et al., 1998)

Enhancer of

Statement

Reference

BacA\p35^GMR.PH, Scer\GAL4^He.PZ, dl¹ is an enhancer of hemocyte phenotype of Dif¹

(Matova and Anderson, 2006)

dl[+]/dl¹ is an enhancer of embryonic epidermis phenotype of cact^E10

(Wakabayashi-Ito et al., 2001)

Suppressor of

Statement

Reference

Scer\GAL4^e33C, dl^UASp.cMa, dl¹ is a suppressor of hemocyte phenotype of Dif¹

(Matova and Anderson, 2006)

Scer\GAL4^e33C, dl^UASp.cMa, dl¹ is a suppressor of hemolymph phenotype of Dif¹

(Matova and Anderson, 2006)

dl^UASp.cMa, Scer\GAL4^He.PZ, dl¹ is a suppressor of hemocyte phenotype of Dif¹

(Matova and Anderson, 2006)

dl^UASp.cMa, Scer\GAL4^He.PZ, dl¹ is a suppressor of hemolymph phenotype of Dif¹

(Matova and Anderson, 2006)

dl^UASp.cMa, Scer\GAL4^srp.Hemo, dl¹ is a suppressor of hemocyte phenotype of Dif¹

(Matova and Anderson, 2006)

dl^UASp.cMa, Scer\GAL4^srp.Hemo, dl¹ is a suppressor of hemolymph phenotype of Dif¹

(Matova and Anderson, 2006)

Df(2L)J4/dl¹ is a suppressor | partially of hemocyte | increased number phenotype of lwr⁵/lwr^4-3

(Chiu et al., 2005)

Df(2L)J4/dl¹ is a suppressor | partially of embryonic/larval plasmatocyte | increased number phenotype of lwr⁵/lwr^4-3

(Huang et al., 2005)

Df(2L)J4/dl¹ is a suppressor | partially of embryonic/larval hemocyte | increased number phenotype of lwr⁵/lwr^4-3

(Huang et al., 2005)

NOT Suppressor of

Statement

Reference

dl¹ is a non-suppressor of embryonic/larval neuromuscular junction phenotype of Ank2^f02001

(Keller et al., 2011)

Df(2L)J4/dl¹ is a non-suppressor of lamellocyte | increased number phenotype of lwr⁵/lwr^4-3

(Chiu et al., 2005, Huang et al., 2005)

Other

Statement

Reference

Dif¹, dl¹ has hemocyte phenotype

(Matova and Anderson, 2006)

Dif¹, dl¹ has hemolymph phenotype

(Matova and Anderson, 2006)

dl¹, fog^hs.PM has embryo phenotype

(Morize et al., 1998)

Additional Comments

Genetic Interactions

Statement

Reference

Homozygous dl¹ does not suppress the NMJ degeneration seen in Ank2^f02001 mutant larvae.

(Keller et al., 2011)

An increased proportion of embryos maternally mutant for Dip3¹ and dl¹/+ show D\V patterning defects compared to dl¹/+ alone. Loss of paternal Dip3 has no effect on the dl¹/+ phenotype.

(Ratnaparkhi et al., 2008)

Rel^E20 dl¹ double mutant larvae are smaller than wild-type, and about half of the double homozygotes die before reaching adult stages.

Dif¹ dl¹ double mutants are small and sluggish and only 3.4% survive to adult. Unchallenged Dif¹ dl¹ double mutant larvae contain many bacteria and yeast in their haemolymph (as many as 10⁵ microbes per animal), while no microbes are observed in wild-type haemolymph. In microbe-free conditions, in the presence of antibiotics, approximately 33% of Dif¹ dl¹ double mutants survive to adult stages, thats a 10-fold increase compared to normal conditions. Dif¹ dl¹ double mutants are able to mount a humoral immune response, but this does not prevent constitutive infection of these animals.

Dif¹ dl¹/+ + double heterozygotes exhibit approximately 5000 blood cells per υl of haemolymph, the same as in wild-type flies. In contrast, Dif¹ dl¹ double homozygotes exhibit a greatly reduced number of haemocytes, approximately 500 per υl - 10-fold fewer than in wild-type. Approximately 15% of Dif¹ dl¹ haemocytes undergo apoptosis, compared with only 2.3% in wild-type.

The few blood cells present in Dif¹ dl¹ mutants exhibit an abnormal morphology. In contrast to wild-type haemocytes, Dif¹ dl¹ blood cells are enlarged, containing intact intracellular bacteria that are not localised to vacuoles and have not been digested. When Dif¹ dl¹ larvae are grown on minimal medium in the presence of antibiotics, the number of haemocytes increases 3-fold, to approximately 1400 cells per υl, and the haemocytes are of normal morphology.

Dif¹ dl¹ animals, in which BacA\p35^GMR.PH is expressed in the haemocytes, under the control of Scer\GAL4^He.PZ still have microbes in the haemolymph, even though the microbial load is 100-fold lower than in Dif¹ dl¹ larvae. After injection with E.coli, nearly all of the BacA\p35^GMR.PH expressing Dif¹ dl¹ larvae become flaccid and die with in a few hours. At 5 hours post infection, the few surviving animals exhibit up to 1000 times more bacteria per animal than wild-type larvae. Bacteria are engulfed by the BacA\p35^GMR.PH-rescued haemocytes but are not digested, subsequently, many of the haemocytes rupture.

Ubiquitous expression of dl^Scer\UAS.cMa, driven by Scer\GAL4^hs.PB at 25^oC (without heat shock) fully rescues the lethality of Dif¹ dl¹ double mutants.

Ubiquitous expression of Dif^Scer\UAS.cIa, driven by Scer\GAL4^hs.PB at 25^oC (without heat shock) fully rescues the lethality of Dif¹ dl¹ double mutants.

Expression of dl^Scer\UAS.cMa in circulating haemocytes, lymph glands, and epidermis, but not in the fat body, under the control of Scer\GAL4^e33C, restores normal haemocyte numbers in Dif¹ dl¹ double mutants. The rescued blood cells are indistinguishable in morphology from wild-type uninfected haemocytes. In addition, the rescued animals have do not have any microbes in their haemolymph and 66% survive to adult stages.

Expression of dl^Scer\UAS.cMa in circulating haemocytes, but not in other immune-responsive tissues, under the control of Scer\GAL4^He.PZ, results in an absence of microbes from the haemolymph, with approximately 45% of dl^Scer\UAS.cMa expressing Dif¹ dl¹ double mutants surviving till adulthood.

Expression of dl^Scer\UAS.cMa in circulating haemocytes and lymph gland cells, under the control of Scer\GAL4^srp.Hemo, increases blood cell number to approximately 90% of wild-type in Dif¹ dl¹ double mutants and enables approximately 50% survival till adulthood. The majority of these larvae have no microbes in their haemolymph.

(Matova and Anderson, 2006)

The melanotic tumour penetrance and circulating hemocyte levels are partially reduced in lwr^4-3 Df(2L)J4/lwr⁵ dl¹ double mutants compared to lwr^4-3/lwr⁵ single mutants. However, the amount of lamellocytes is not reduced.

(Chiu et al., 2005)

In lwr^4-3/lwr⁵; dl¹/Df(2L)J4, total numbers of hemocytes are reduced compared to lwr^4-3/lwr⁵ single mutants. Plasmatocyte levels are reduced by 50% compared to single mutants, while lamellocyte levels are not significantly reduced.

(Huang et al., 2005)

95% of twi¹/+; dl¹/+ animals raised at 18^oC survive to adulthood whereas only 0.6% of those raised at 25^oC do. This temperature sensitive lethality is not significantly affected by the presence or absence of sc^M6/+ or sc^+t.XSE.

(Wrischnik et al., 2003)

All embryos laid by cact^E10/+, dl¹/+ females are weakly dorsalized.

(Wakabayashi-Ito et al., 2001)

Embryos carrying fog^hs.PM show a flattened stretched appearance around their entire circumference and disorganisation of the ordered arrangement of cells.

(Morize et al., 1998)

The zygotic semi-lethality of cact⁷ homozygotes is not suppressed by dl¹.

(Qiu et al., 1998)

A partial restoration of cuticle pattern elements along the dorso-ventral axis is seen in embryos derived from dl¹ females if the females also carry Dif^bcd.PS. The degree of ventralisation seen in these rescued embryos is increased if the females are also heterozygous for cact⁷. The gastrulation defects of embryos derived from dl¹ females is partially rescued if the females also carry Dif^bcd.PS; anterior movement of the posterior midgut invagination is seen along the dorsal side of the embryo, but the ventral furrow does not form.

(Stein et al., 1998)

Double mutant combinations with ea^D1 are strongly dorsalizing.

(Chasan et al., 1992)

Xenogenetic Interactions

Statement

Reference

The degree of lethality of embryos derived from dl¹/+ females at 29[o]C is not significantly altered if the females are expressing of one copy of Zzzz\Pvank1^{Scer\UAS.T:Zzzz\FLAG} under the control of Scer\GAL4^{mat.αTub67C.T:Hsim\VP16}. However, if the females are expressing two copies of Zzzz\Pvank1^{Scer\UAS.T:Zzzz\FLAG}, the fraction of embryos failing to hatch is increased, and the degree of dorsalisation of the unhatched embryos is more severe.

The degree of lethality of embryos derived from dl¹/+ females at 29[o]C is not significantly altered if the females are expressing of one copy of Zzzz\I2vank3^{Scer\UAS.T:Zzzz\FLAG} under the control of Scer\GAL4^{mat.αTub67C.T:Hsim\VP16}. However, if the females are expressing two copies of Zzzz\I2vank3^{Scer\UAS.T:Zzzz\FLAG}, the fraction of embryos failing to hatch is increased, and the degree of dorsalisation of the unhatched embryos is more severe.

(Gueguen et al., 2013)

Expression of BacA\p35^GMR.PH in the haemocytes, under the control of Scer\GAL4^He.PZ in Dif¹ dl¹ animals results in the number of blood cells per υl of haemolymph increasing 4-fold, to approximately 2200 cells per υl, whereas the blood cell number remains constant in Dif¹ dl¹ heterozygotes.

(Matova and Anderson, 2006)

Complementation and Rescue Data

Fails to complement

dl^D447

(Minidorff et al., 2007)

dl^C447

(Minidorff et al., 2007)

Rescued by

dl¹ is rescued by dl^bcd.PB

(Briggs et al., 1998)

Partially rescued by

dl¹ is partially rescued by dl^UASp.cRa/Scer\GAL4^{VP16.mat.αTub67C}

(Ratnaparkhi et al., 2006)

dl¹ is partially rescued by dl^VP16.UASp/Scer\GAL4^{VP16.mat.αTub67C}

(Ratnaparkhi et al., 2006)

dl¹ is partially rescued by dl^p65.UASp/Scer\GAL4^{VP16.mat.αTub67C}

(Ratnaparkhi et al., 2006)

dl¹ is partially rescued by dl^Tag:nt1

(Jia et al., 2002)

dl¹ is partially rescued by dl^{M4prime.Tag:nt1}

(Jia et al., 2002)

dl¹ is partially rescued by dl^{M7prime.Tag:nt1}

(Jia et al., 2002)

dl¹ is partially rescued by dl^M8.Tag:nt1

(Jia et al., 2002)

dl¹ is partially rescued by dl^M16.Tag:nt1

(Jia et al., 2002)

dl¹ is partially rescued by dl^380.Tag:nt1

(Jia et al., 2002)

dl¹ is partially rescued by dl^Glu312.bcd

(Briggs et al., 1998)

dl¹ is partially rescued by dl^NLS.bcd

(Briggs et al., 1998)

dl¹ is partially rescued by dl^Ala312.bcd

(Briggs et al., 1998)

Not rescued by

dl¹ is not rescued by dl^M2.Tag:nt1

(Jia et al., 2002)

dl¹ is not rescued by dl^M18.Tag:nt1

(Jia et al., 2002)

dl¹ is not rescued by dl^M20.Tag:nt1

(Jia et al., 2002)

dl¹ is not rescued by dl^M23.Tag:nt1

(Jia et al., 2002)

Comments

dl^T:boss-NT1 rescues the ventral denticle belts and Filzkorper and partially restores the head skeleton in embryos derived from dl¹ females. However, the head is abnormal and hatching is not seen.

dl^{M16.T:boss-NT1} partially rescues the cuticle phenotype of embryos derived from dl¹ females.

The cuticle phenotype of embryos derived from dl¹ females is not rescued by dl^{M2.T:boss-NT1}, dl^{M18.T:boss-NT1}, dl^{M20.T:boss-NT1} or dl^{M23.T:boss-NT1}.

The cuticle phenotype of embryos derived from dl¹ females is only weakly rescued by dl^{M4prime.T:boss-NT1}, dl^{M7prime.T:boss-NT1} or dl^{M8.T:boss-NT1}.

dl^{380.T:boss-NT1} rescues the Filzkorper but not the ventral denticle belts in embryos derived from dl¹ females.

(Jia et al., 2002)

Images (0)

Mutant

Wild-type

Stocks (4)

Bloomington

3236

dl¹ cn¹ sca¹/CyO, l(2)DTS100¹