|Feature type||allele||Associated gene||Dmel\htl|
|Map ( GBrowse )|
|Allele class||amorphic allele - genetic evidence, loss of function allele|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Amino acid replacement: R276@. Nucleotide substitution: C935T. Mutant residue is just amino-terminal to the transmembrane domain.
|Phenotype Manifest In|
axon & mechanosensory neuron & adult head (with htlYY262), with Scer\GAL4Bx-MS1096, Scer\GAL4Mz1277, Scer\GAL4twi.PB, htlScer\UAS.cMa
axon & ocellus sensory structure (with htlYY262), with Scer\GAL4Bx-MS1096, Scer\GAL4Mz1277, Scer\GAL4twi.PB, htlScer\UAS.cMa
Many of the LVM founder cells present in htl[AB42] mutant stage 12 embryos lose contact with the trunk visceral mesoderm (TVM) rather than spreading out across it. By stage 13 a large number of rounded and shrunken cells are seen some distance from the TVM.
Stage 11 and 12 mutant embryos have an abnormally shaped cardiogenic mesoderm.
Homozygous glial cell clones in the eye disc are only slightly smaller than wild-type clones, and the mutant cells migrate normally. The mutant clones comprise all glial cell types. However, the mutant cells do not adopt the typical wrapping phenotype, but instead are thin and spindle-shaped.
Homozygous embryos show defects in mesoderm spreading during stage 8, which results in the mesoderm forming a multilayered structure at stages 9-10 (in contrast to wild-type embryos where the mesoderm forms a single layer of cells at this stage).
Mutant embryos show mesoderm cell defects that affect both collapse of the ventral furrow and spreading in the angular direction during gastrulation. The angular movement of upper furrow cells is strongly affected in the mutants. The last cells to invaginate in the mutant embryos, which make up the lower furrow, behave in a similar manner to wild-type furrow cells.
In htlAB42 embryos, the ventral cord is largely uncondensed compared to wild type. The migration of hemocytes during embryonic development appears normal. This phenotype is fully penetrant.
Late stage mutant embryos show variable defects in the shape and location of the corpus cardiacum, from almost normal to stretched out and shifted posteriorly.
In stage-15 htlAB42 mutant embryos, the lymph gland, cardioblasts and pericardial nephrocytes fails to develop from the cardiogenic mesoderm.
htl[AB42] mutants exhibit defects in longitudinal visceral muscles. Morphology appears grossly normal in stage 11 and early stage 12 embryos. Longitudinal visceral muscle fibers are all but absent in stage 13 htl[AB42] mutant embryos, although circular fiber precursors are essentially normal. The amount of apoptotic cell death is generally increased in htl[AB42] mutants.
Cell shape changes in the migrating mesoderm after invagination fail to occur in htlAB42 homozygous embryos. Initially, the mesodermal epithelial tube extends further into the interior of the embryo when compared with wild type. Then, following mitosis in the invaginated mesoderm, the leading edge cells fail to extend dorsolaterally. Some migration does eventually take place and mesodermal cells do undergo some protrusive activity, but they fail to form a monolayer as in wild-type. As a result of these defects, by stage 10-12 there are no eve positive mesodermal cells in any hemisegment. In htlAB42 homozygous embryo, cells at the base of the mesodermal tube at stage 7 fail to attach to underlying ectodermal cells and fail to align along the ventral midline. As in wild-type mesoderm, adherens junctions are lost from the mesoderm in htlAB42 homozygotes after invagination.
No increase is seen in cardioblast numbers in the developing embryo.
Salivary gland shape and position is abnormal in homozygous and htlAB42/htlEMS2 embryos. The visceral mesoderm is disrupted in mutant embryos, showing gaps of variable width.
Pericardial cells fail to form in mutant embryos, due to defects in mesoderm migration.
Homozygous mutants display a defect in mesodermal cell migration. Embryos display an irregular layer where mesodermal cells remain clustered and fail to undergo their complete dorsal migration.
The abnormal pathfinding behaviour in ocellar pioneer (OP) and bristle mechanosensory axons (BM) seen in individuals expressing htlDN.Scer\UAS.cMb under the control of Scer\GAL4sca-537.4 are enhanced by the addition of htlAB42. htlYY262/htlAB42 flies rescued to the pupal stage by expression of htlScer\UAS.cMa under the control of three drivers (Scer\GAL4Mz1277, Scer\GAL4Bx-MS1096 and Scer\GAL4twi.PB) gives axon guidance phenotypes in the head. Ocellar pioneer (OP) axons project into the epidermis, bristle mechanosensory (BM) axons fail to project into the brain, or stall in the epidermis or extend apart of epidermis.
Homozygous clones in the eye are wild-type.
Most of the cardial and dorsal somatic muscle cells fail in their dorsal migrations in htlAB42 embryos.
Migration of the mesoderm fails to occur properly in homozygous embryos.
The mesodermal cells fail to undergo their normal dorsolateral migration in homozygous embryos and the cells remain aggregated instead of forming a monolayer. Later stage embryos show almost complete loss of cardial and pericardial cells and a marked reduction in the number of dorsal, lateral and ventral groups of somatic muscles. The failure of mesodermal migration is fully rescued by htlScer\UAS.cMa expressed under the control of Scer\GAL4twi.PG.
Mesoderm cells remain close to the ventral midline rather than migrating towards the dorsal ectoderm in homozygous embryos. All eve-positive mesodermal cells are missing. Most of the dorsal somatic muscles, cardial and pericardial cells fail to form. Large gaps are seen in the visceral mesoderm.
Defect in cardiac development, residual pericardial cells are randomly distributed. Most of the dorsal somatic muscles are entirely missing and gaps are seen in the lateral and ventral muscle groups as well, there is both an increasing severity and variability in muscle loss from ventral to dorsal positions of embryos. Visceral musculature fails to undergo its normal morphogenesis (constrictions are not formed). Embryonic mesoderm appears as a multilayed collection of cells on either side of the extended germ band instead of a monolayer beneath the ectoderm.
|Phenotype Manifest In|
htlAB42 has embryonic pericardial cell phenotype, suppressible | partially by btl::htlHB.Scer\UAS/Scer\GAL4twi.PG
htlAB42 has embryonic pericardial cell phenotype, suppressible | partially by htl::torScer\UAS.cDa/Scer\GAL4twi.PG
htlAB42 has embryonic pericardial cell phenotype, suppressible | partially by Scer\GAL4twi.PG/Egfr::htlScer\UAS.cDa
htlAB42 has longitudinal visceral muscle primordium | embryonic stage 12 phenotype, suppressible | partially by Scer\GAL4tey-5053A/BacA\p35Scer\UAS.cHa
htlAB42 has longitudinal visceral muscle primordium | embryonic stage 13 phenotype, suppressible | partially by Scer\GAL4tey-5053A/BacA\p35Scer\UAS.cHa
htlAB42 has mesoderm phenotype, suppressible | partially by Scer\GAL4twi.PG/btl::EgfrScer\UAS.T:λ\cI-DD
|NOT suppressed by|
|NOT Enhancer of|
Expression of btlScer\UAS.T:λ\cI-DD under the control of Scer\GAL4twi.PG is able to induce bilaterally symmetrical flattening of the mesodermal tube onto the ectoderm in htlAB42 embryos. Expression of either btl::EgfrScer\UAS.T:λ\cI-DD or PvrScer\UAS.T:λ\cI-DD under the control of Scer\GAL4twi.PG is not able to rescue either early contact between the mesoderm and ectoderm or symmetric flattening of the mesodermal tube in the early stages of mesoderm morphogenesis in htlAB42 embryos.
Expression of btl::htlHB.Scer\UAS or Egfr::htlScer\UAS.cDa under the control of Scer\GAL4twi.PG in htlAB42 embryos partially rescues pericardial cell development; in most cases only 12 to 18 (instead of 20) pericardial cells are properly determined and they often form small clusters instead of being aligned along the anterior-posterior axis. Expression of htl::torScer\UAS.cDa under the control of Scer\GAL4twi.PG in htlAB42 embryos results in the formation of excess pericardial cells.
Embryos heterozygous for htlAB42 and ush1 show a strong mesodermal migration defect. Also about half show a loss of cells from the dorsal mesoderm.
The failure of mesodermal migration is partially rescued by Ras85DG13Q.Scer\UAS expressed under the control of Scer\GAL4twi.PG.
Expression of BacA\p35[Scer\UAS.cHa] under the control of Scer\GAL4[tey-5053A] partially suppresses the longitudinal visceral muscle (LVM) founder cell migration and survival defects seen in homozygous htl[AB42] stage 12/13 embryos. LVM founder cells regain much of the ability to migrate, however their tracks towards the anterior of the embryo are less efficient than in wild type with cells seen veering off in dorsal and ventral directions.
|Complementation & Rescue Data|
|Fails to complement|
|Partially rescued by|
|Not rescued by|
Expression of htl[Scer\UAS.cMa] under the control of Scer\GAL4[tey-5053A] rescues the longitudinal visceral muscle (LVM) founder cell death seen in htl[AB42] mutant stage 13 embryos. The founder cell migration defects are also partially rescued, however some cells acquire abnormal shapes, adhere to positions more distant from the TVM both dorsally and ventrally, and form clusters, resulting in missing LVM cells in the most anterior trunk segments. Expression of htl[Scer\UAS.T:λ\cI-DD] under the control of Scer\GAL4[tey-5053A] rescues the longitudinal visceral muscle (LVM) founder cell death seen in htl[AB42] mutant stage 13 embryos. The founder cell migration defects are also partially rescued, however some cells acquire abnormal shapes, adhere to positions more distant from the TVM both dorsally and ventrally, and form clusters, resulting in missing LVM cells in the most anterior trunk segments.
htlScer\UAS.cMa; Scer\GAL4twi.PB rescues the migration of the mesoderm after invagination in htlAB42 embryos. As a result the number of hemisegments with eve expressing mesodermal cells is 22, just as in wild-type. In contrast, htlScer\UAS.T:λ\cI-DD ; Scer\GAL4twi.PB rescues the migration of the mesoderm after invagination in htlAB42 embryos, but only partially rescues differentiation of the mesoderm (an average of 12.2 hemisegments per embryo have eve expressing mesodermal cells.
The addition of htlScer\UAS.cMa driven by Scer\GAL4twi.PB, fails to rescue the lethality seen in htlYY262/htlAB42. However, when htlScer\UAS.cMa is driven by Scer\GAL4Mz1277, Scer\GAL4Bx-MS1096 and Scer\GAL4twi.PB concurrently, some escaper pupae do survive.
|Stocks ( 1 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 4 )|
|Secondary FlyBase IDs|
|References ( 29 )|
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|Recent research papers ( 3 )|