|Feature type||allele||Associated gene||Dmel\ems|
|Also Known As||ems9Q64, ems9Q|
|Map ( GBrowse )|
|Allele class||amorphic allele - genetic evidence|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
stop codon at residue 141
|Phenotype Manifest In|
ems mutant MARCM clones exhibit neuronal loss specifically in the lateral neuroblasts in the 1Nb lineage. This results in a marked reduction in the size of the antennal lobes.
Homozygous and wild-type anterodorsal projection neuron (adPN) clones are recovered with equal frequency (clones induced in early first instar larvae and analysed in late third instar larvae). The average number of cells in homozygous and wild-type adPN clones is virtually identical. Homozygous lateral projection neuron (lPN) clones are recovered at a much lower frequency than wild-type lPN clones (in 2% versus 25% of brains) (clones induced in early first instar larvae and analysed in late third instar larvae). Homozygous lPN clones are much smaller in size (containing fewer cells) than wild-type lPN clones. Homozygous adPN neuroblast clones (induced in the early first instar larva and analysed in the adult brain) show normal cell body projection and axonal projection trajectory, but show marked defects in dendritic targeting, with three types of phenotype being observed. Firstly, mutant adPNs fail to innervate specific glomeruli that are always innervated by wild-type adPNs; the VA1lm glomerulus is innervated by mutant adPNS in only 63% of clones, VA3 in only 71% of clones and VM2 in only 83% of clones. Secondly, mutant adPNs are seen to ectopically innervate inappropriate glomeruli; the DL2 glomerulus is ectopically innervated in 71% of clones, DA2 in 29%, VA6 in 21%, DL5 in 21%, VL2 in 54%, VM1 in 17%, DA1 in 37%, DA4 in 54% and DC1 in 42%. Thirdly, mutant adPNs form inappropriate misprojections into the subesophageal ganglion (this phenotype is seen in approximately one-third of the mutant clones). The axons of homozygous adPN neuroblast clones (induced in the early larva and analysed in the adult) project a fascicle to the lateral horn and form two arborization areas comparable to those of the wild type. Single cell homozygous clones of DL1-innervating adPNs correctly innervate the DL1 glomerulus, project their axons to the lateral horn, bifurcate and form two wild-type-like terminal processes.
ems3 mutant brain neuroblast clones induced during the early first instar contain a similar number of cells to wild-type clones at 48 hours after larval hatching (ALH). However, at 72 hours ALH the ems3 mutant clones contain fewer cells than wild-type clones. This difference increase at 96 hours ALH and remains large throughout pupal development and in the adult. BrdU staining shows that the decrease in cell number in ems3 clones is not due to reduced cell proliferation. When examined in the adult brain, many ems3 mutant clones lack the prominent protocerebral fascicle that projects to the superior medial protocerebrum in the wild-type control. In other clones, a reduced protocerebral fascicle is formed. In all clones examined, aberrant projections extend without obvious pattern towards adjacent neuropiles. Misdirected projections of this type are also present in larval ems3 clones. Studies of single cell ems3 MARCM clones shows that these cells fail to extend correct neurite projections and therefore have a cell-autonomous requirement for ems.
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.
ScrC1 AntpNs-rvC3 UbxMX2 abd-AM1 Abd-BM8 larvae (deficient for activity of thoracic and abdominal homeotic genes) exhibit sclerotic plates (sp) anterior to each denticle belt. Differentiation of sp depends on ems+ function.
The Bolwig organ, dorso-medial and lateral papillae, dorsal organ and associated organ are absent in homozygous embryos. The oesophageal ganglion is reduced in size. The optic lobes are reduced in size and are found in a posterior instead of ventral position in older embryos.
Mandibular segment, intercalary segments, antennal segments, associated organ, Bolwig's organ, dorsomedial papilla, antennal sense organ and dorsolateral papilla are deleted. Stomatogastric nervous system is present.
ems3 has increased cell death | somatic clone phenotype, suppressible by Scer\GAL4αTub84B.PL/BacA\p35Scer\UAS.cHa
ems3 has neuroanatomy defective | somatic clone | adult stage phenotype, suppressible | partially by acj61,4.Scer\UAS/Scer\GAL4GH146
|Phenotype Manifest In|
ems3 has adult antennal lobe projection neuron VA1v adPN | somatic clone phenotype, suppressible by acj61,4.Scer\UAS/Scer\GAL4GH146
ems3 has antennal lobe projection neuron lPN | somatic clone phenotype, suppressible | partially by Scer\GAL4αTub84B.PL/BacA\p35Scer\UAS.cHa
|NOT suppressed by|
ems3 has adult antennal lobe projection neuron VA3 adPN | somatic clone phenotype, non-suppressible by acj61,4.Scer\UAS/Scer\GAL4GH146
Expression of acj6[1,4.Scer\UAS] under the control of Scer\GAL4[GH146] in homozygous ems adPN neuroblast clones (induced in the early larva and analysed in the adult) significantly rescues the innervation defects of the VA1lm glomerulus, but does not significantly rescue the innervation defects of the VA3 and VM2 glomeruli which are seen in single mutant homozygous ems adPN neuroblast clones.
The reduced recovery of ems lateral projection neuron (lPN) clones is rescued to a wild-type recovery rate if the clones are also expressing BacA\p35[Scer\UAS.cHa] under the control of Scer\GAL4[αTub84B.PL]. The average number of cells in these rescued lPN clones corresponds to 71% of the cell number seen in wild-type clones.
|Complementation & Rescue Data|
|Stocks ( 0 )|
|Notes on Origin|
Jurgens, Wieschaus, Nusslein-Volhard and Kluding, 1984.
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 4 )|
|Secondary FlyBase IDs|
|References ( 15 )|