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General Information
Symbol
Dmel\Tl10b
Species
D. melanogaster
Name
FlyBase ID
FBal0016833
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Toll10b, TlD, Toll10b
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

G26840195A

Amino acid change:

C781Y | Tl-PB; C781Y | Tl-PC; C781Y | Tl-PD

Reported amino acid change:

C781Y

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change. Mutated residue is located on the external surface near the transmembrane spanning domain.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Amino acid replacement: C781Y. Residue is located on the external surface near the transmembrane spanning domain.

Amino acid replacement. Mutation is in the extracellular domain.

Amino acid replacement.

Nucleotide substitution: G2916A. Amino acid replacement: C781Y. This mutation is in the extracellular domain of the protein.

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
Phenotype Manifest In
Detailed Description
Statement
Reference

Heterozygous third instar larvae have melanotic nodules found in the hemocoel or in association with He-positive lymph glands.

Mutant larvae show abnormal lamellocyte differentiation in the secondary lymph gland lobes, resulting in a dramatic enlargement of the secondary lymph gland lobes.

The number of hemocytes in the hemolymph of Tl8 mutant larvae is significantly higher than in wild type and the number of lamellocytes is increased within the hemocyte pool. Most aggregated hemocytes consist of lamellocytes that are partially to fully melanized. Mitotic analyses of hemocytes show that lamellocytes do not divide in circulation so the excess number must be due to proliferation in the lymph gland. However, plasmatocytes and prohemocytes do divide in circulation in Tl8 mutants, while no such division occurs in wild type.

Tl8 mutant flies exhibit increased susceptibility to DXV virus infection compared to wild-type. These flies also demonstrate early onset of anoxia sensitivity, while exhibiting a viral load approximately 50% that of wild-type flies at the same time point.

The cuticle is completely absent in mutant larvae.

Mutant females generate ventralised embryos.

The concentration of circulating hemocytes in heterozygous larvae is increased compared to controls. The fraction of podocytes and lamellocytes is increased compared to controls.

Mutant embryos differentiate almost exclusively as somatic mesoderm.

Lamellocytes appear in circulation during the second instar stage in mutants and are abundant in the hemolymph of third instar larvae (5-25%), where they participate in the formation of melanotic tumours. The crystal cell population is not affected. Lamellocytes are not present in the lymph glands of third instar mutant larvae.

Heterozygous larvae contain free-floating melanotic masses. These masses are surrounded by several layers of lamellocytes.

Less than 1% of heterozygous adults have melanotic capsules. Hemocyte density in the hemolymph of Tl8/+ larvae is significantly higher than in the hemolymph of control larvae. The number of dividing hemocytes in the hemolymph is significantly higher than in wild-type.

In the absence of immune challenge the antifungal gene Drs is constitutively expressed.

Abnormal fat body morphology. P{Dipt2.2-lacZ} is not induced in heterozygous larvae.

Cell intercalation in lateralized Tl mutant embryos proceeds normally during germ band extension.

Injecting transcripts from Tl8 into dorsalized spz4 mutant embryos causes ventralization near the site of injection indicating that Tl acts downstream of spz.

Additional dl protein in gain of function dorsal group backgrounds shifts the nuclear dl gradient ventrally.

Ventralised embryos, the mesoderm is expanded so little or no epidermis is made.

Strongly ventralized embryos: blastomeres behave as mesodermal cells. Altered pattern of dpp and zen. Heterozygotes show normal twi and sna expression patterns along dorsoventral axis.

Embryos from heterozygous females are extremely ventralised; the mesoderm is expanded. Females carrying Tl8 in trans with a null allele of Tl produce ventralised embryos.

Embryos derived from Tl8 females are variably ventralised. At the late cellular blastoderm stage, all the cells have flattened apical surfaces and the nuclei have moved inwards towards the centre of the embryo. Incompletely ventralised embryos show abnormalities in ventral furrow formation, with the furrow generally being larger than in wild-type.

Female viability and male fertility are not reduced. Embryos exhibit ventralised phenotype.

dominant

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement
Reference
NOT Enhancer of
Statement
Reference

Tl10b is a non-enhancer of visible phenotype of upd1GMR.PB

NOT Suppressor of
Statement
Reference

Tl10b is a non-suppressor of visible phenotype of upd1GMR.PB

Other
Statement
Reference
Phenotype Manifest In
Suppressed by
Statement
Reference

Tl10b has lamellocyte phenotype, suppressible by Stat92E[+]/Stat92E06346

Tl10b has podocyte phenotype, suppressible by Stat92E[+]/Stat92E06346

NOT suppressed by
Statement
Reference

Tl10b has lamellocyte phenotype, non-suppressible by brm[+]/brm2

Tl10b has plasmatocyte phenotype, non-suppressible by brm[+]/brm2

Tl10b has podocyte phenotype, non-suppressible by brm[+]/brm2

Tl10b has embryonic/larval hemocyte phenotype, non-suppressible by brm[+]/brm2

Tl10b has embryonic/larval hemocyte phenotype, non-suppressible by Stat92E[+]/Stat92E06346

NOT Enhancer of
Statement
Reference

Tl10b is a non-enhancer of eye phenotype of upd1GMR.PB

NOT Suppressor of
Statement
Reference

Tl10b is a non-suppressor of eye phenotype of upd1GMR.PB

Tl10b is a non-suppressor of denticle belt phenotype of Myd88c03881

Tl10b is a non-suppressor of filzkorper phenotype of Myd88c03881

Other
Statement
Reference

Tl10b, cact3/cact[+] has melanotic mass phenotype

Additional Comments
Genetic Interactions
Statement
Reference

Abnormal differentiation of lamellocytes is not seen in the secondary lymph gland lobes of Tl8 MybMH107 double mutant larvae. The lymph gland hemocytes fail to overproliferate in the double mutant larvae.

The increased concentration of circulating hemocytes seen in Tl8/+ larvae is not suppressed by Stat92E06346/+, but the increased numbers of podocytes and lamellocytes seen in Tl8/+ larvae are strongly suppressed by Stat92E06346/+. The concentration of circulating hemocytes in mxcG43/Y ; Tl8/+ larvae is less than the number seen in either single mutant.

Tl8/+ ; domk08108 double mutant larvae contain melanotic masses, although their frequency is markedly reduced compared to Tl8/+ single mutant larvae and the masses are devoid of hemocytes.

50.9% of cact3/+ ; Tl8/+ adults have melanotic capsules.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
Comments
Comments

Tl8 maps between e and ca.

Class I allele.

Class I Tl allele.

Constitutively active receptor, so dl undergoes nuclear translocation along the entire dorsoventral circumference.

Constitutively active protein.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (10)
Reported As
Symbol Synonym
Tl8
toll10B
Secondary FlyBase IDs
    References (116)