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General Information
Symbol
Dmel\ems2
Species
D. melanogaster
Name
FlyBase ID
FBal0003713
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
ems9H83, ems9H
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

C13902659T

Amino acid change:

Q161term | ems-PA

Reported amino acid change:

Q161term

Comment:

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

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

stop codon at residue 161

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

56% of mutant embryos show brain defects; the brain has a deletion in the deutocerebral and tritocerebral brain anlagen, which leads to a prominent gap devoid of neuronal cells between the remaining protocerebral brain hemispheres and the subesophageal neuromeres.

66% of mutant embryos have an "open-head" phenotype in which the anterodorsal head ectoderm is defective. Head involution is perturbed and brain hemispheres protrude out of the embryo at the gap in the dorsal head.

The tracheal placodes are slightly smaller than normal in mutant embryos. The visceral branches of the tracheal system generally fail to form. Occasionally, the ganglionic or dorsal branches appear truncated.

In an ems2 mutant the ems staining interneurons in the ventral nerve cord do not extend axons across the midline and turn rostrally during stages 13-14 as seen in wild-type.

The stigmatophore protrudes normally but the spiracular chamber is defective in that it lacks a filzkorper and is not connected to the trachea. The stigma in developing embryos fails to slide posteriorly, a phenotype similar to that seen in Abd-BM1 mutants. The spiracle cells that are in contact with the trachea fail to invaginate, perhaps causing the failure of posterior sliding of the developing stigmatophore.

Neuromeres b2 and 3 are absent or reduced in all embryos.

Fail to develop filzkorper and the remaining spiracular structures are intact.

Embryos have no Dll expression in the antennae primordium, it is expressed in other limb primordium. Intercalary and antennal segments and a portion of the pre-antennal region defined by the en head spot are absent in ems mutant embryos.

Absence of head structures.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement
Reference
Phenotype Manifest In
Suppressed by
Statement
Reference
NOT suppressed by
Other
Additional Comments
Genetic Interactions
Statement
Reference

Expression of ocScer\UAS.cBa under the control of Scer\GAL4sca-537.4 does not significantly rescue the embryonic brain defects or the "open-head" ectoderm defects of ems2 mutants.

Quadruple ctdb7, Df(2L)32FP-5 (deficiency for sal), ems2, domeG0468 mutants are missing spiracle structures completely.

Xenogenetic Interactions
Statement
Reference

Expression of Zzzz\emxScer\UAS.cHa under the control of Scer\GAL4sca-537.4 does not result in a significant rescue of the embryonic brain defects of ems2 mutants, but there is significant rescue of the "open-head" ectoderm defects of ems2 mutants in these animals.

Expression of Zzzz\emx+hp.Scer\UAS under the control of Scer\GAL4sca-537.4 does not result in a significant rescue of the embryonic brain defects of ems2 mutants.

Heatshocked induced ubiquitous expression of Mmus\Emx2hs.PH in ems2 null mutants leads to substantial restoration of brain morphology. In a quarter of cases the cellular gap and the longitudinal ganglion are restored, however projection defects are not rescued.

Complementation and Rescue Data
Partially rescued by

ems2 is partially rescued by emshs.PH

Comments

Expression of either emsScer\UAS.cRa or ems-hp.Scer\UAS under the control of Scer\GAL4sca-537.4 significantly rescues the embryonic brain defects and the "open-head" ectoderm defects of ems2 mutants.

Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer

Jurgens, Wieschaus, Nusslein-Volhard and Kluding, 1984.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (15)