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FB2026_01
,
released March 12, 2026
11bp deletion: frame shift after 7 amino acids of the wild type protein.
Small deletion which causes a frame shift after the 7th amino acid.
11bp deletion after amino acid 7 leads to a frameshift.
embryonic brain & ganglion mother cell
Stage 15-16 mutant embryos show visceral muscle defects and parts of the hindgut are also missing.
95% of homozygous fkh6 mutant anterior dMP2 neurons fail to undergo apoptosis. At stage 17, dMP2 axons often exit the VNC prematurely or, occasionally, cross the midline.
fkh6 mutants do not develop a foregut. However, this does not affect the formation of the pars intercerebralis.
The stomatogastric nervous system is absent in mutant stage 16 embryos, but the corpus cardiacum is present.
In mutant embryos the ventral midline glia ventral to the foregut are still present.
70% of mutant embryos have defects in the b1 region of the embryonic brain. There is an unusually small space between the brain hemispheres, abnormal defasciculation of the preoral brain commissure and a decrease in the area occupied by neuronal nuclei in the b1 and b2-S3 regions of the embryonic brain. There is also a reduction in the number of glia in the b2-S3 regions of the embryonic brain. At late embryonic stage 13, mutant embryos show a reduction in the number of apoptotic cells at the dorsal midline of the brain compared to wild type. The number of brain ganglionic mother cells in stage 11 mutant embryos is decreased compared to wild type.
Although a normal salivary gland secretory placode is formed in mutant embryos, an invaginating pit is not evident during stage 11, and the secretory cells fail to invaginate. The mutant salivary placode cells are a mixture of round and columnar cells (wild-type salivary placode cells are uniformly columnar), with the ventral-most region consisting mostly of round cells. Many of the mutant cells are found in multiple layers, with some cells apparently dissociating from the salivary epithelium (wild-type secretory cells are always in a monolayer). Numerous macrophage-like cells and pyknotic structures are seen surrounding the salivary primordia in mutant embryos, in contrast to wild type where very few macrophage-like cells and pyknotic structures are seen. Mutant secretory cells in the dorsal-posterior region of the placode have nuclei in a basal position, as in wild-type embryos, but they mostly remain columnar, rather than becoming wedge-shaped, as in wild-type salivary glands. In stage 13 embryos, apoptotic bodies with condensed nuclei and cytoplasm are found within the secretory epithelium. Numerous macrophages that have engulfed apoptotic bodies surround the dying secretory cells.
The normal number of caudal visceral mesoderm cells develop, but they fail to migrate along the trunk visceral mesoderm. By stage 14 most of the caudal visceral mesoderm cells have been eliminated by apoptosis.
During embryogenesis the salivary secretory cells fail to invaginate and eventually disappear. Salivary duct cells also fail to invaginate to form tubes but do occasionally invaginate to form a teardrop-shaped structure.
Physical block to head involution due to improper formation of the foregut and anterior midgut. Involution stops before the labial lobes are completely internalised. Labial sensory organs remain external and become ectopic external sensory organs.
Mutant embryos lack the stomodeal nervous system.
Anal pads and hindgut are missing.
Primordial germ cells exit the gut primordium normally in mutant embryos.
Defective in gonad assembly.
No changes in phenotype of tor13D embryos.
The anterior and posterior midgut primordia begin to degenerate at the end of the extended germband stage and are extensively degenerated in a stage 12 (germband shortening) embryo. No outbudding of the Malpighian tubules is observed. The salivary glands do not invaginate, and ultimately some of the cells which remain at the surface degenerate. The hindgut has an abnormal morphology after germband retraction, forming a short, straight tube.
Failure of head involution. Homeotic transformations in the pre-oral head region and the foregut. Posterior tail region and the hindgut are homeotically replaced by anterior tail and post-oral head. Embryos lack oesophagus, proventriculus, hindgut and Malpighian tubules.
fkh6 has increased cell death phenotype, non-suppressible by Scer\GAL4arm.PS/sensUAS.cNa
Df(3L)H99, fkh6 has abnormal cell shape | embryonic stage 11 phenotype
Df(3L)H99, fkh6 has abnormal endomitotic cell cycle phenotype
fkh6 has embryonic/larval salivary gland phenotype, non-suppressible by Scer\GAL4arm.PS/sensUAS.cNa
Df(3L)H99, fkh6 has salivary gland body primordium | embryonic stage 11 phenotype
Df(3L)H99, fkh6 has embryonic Malpighian tubule phenotype
Df(3L)H99, fkh6 has embryonic salivary gland duct phenotype
Df(3L)H99, fkh6 has presumptive embryonic salivary gland phenotype
byn5, fkh6 has longitudinal trunk visceral muscle primordium phenotype
During stage 11 of embryogenesis, the salivary gland primordium of fkh6, Df(3L)H99 double homozygotes fails to form an invagination pit, exhibits a defective enclosing supra-cellular myosin cable, which only persists along the lateral boundaries, and its cells fail to constrict apically, but the primordium does not exhibit significant differences in circularity, as compared to controls; the region to the anterior of the presumptive invagination site also fails to cluster the primordium cells with lower apical surface area, and these cells also fail to form big apical foci of myosin and of Rok protein, as compared to controls.
The central nervous system cells of fkh6 Df(3L)H99 double mutant embryos undergo normal mitotic cycles throughout embryogenesis and incorporate BrdU (as occurs in wild type). In contrast to wild-type, BrdU incorporation is not seen in endoreplicating cells of the salivary glands, midgut, hindgut and Malpighian tubules in the fkh6 Df(3L)H99 embryos. In additional to the BrdU incorporation defects, the mutant Malpighian tubules are abnormal in morphology. The nuclei of mutant salivary gland cells are consistently smaller than those of their wild-type siblings.
In Df(3L)H99 fkh6/Df(3L)H99 fkh6 embryos, salivary gland cells fail to invaginate, and expression of salivary gland duct markers expands into salivary gland secretory cells. (Note: Df(3L)H99 is present to suppress apoptosis in the salivary gland previously detected in fkh mutant embryos, but not assayed as part of this work.)
Salivary gland secretory cells fail to be internalised in fkh6 ; Df(3L)H99 double mutant embryos. Cells of the double mutant placode are columnar, like wild-type cells, except for cells in the ventral-posterior portion of the placode, which are round and stacked on one another. Coordinate nuclear migration occurs in the secretory cells of all double mutant embryos in approximately the same temporal and spatial pattern as in wild type, but the apical surface membranes fail to constrict even at very late stages. The invaginating pits of double mutant salivary glands are therefore wide and shallow compared to wild type. Fewer apical membrane protrusions are found at the surface of double mutant secretory cells compared to wild type.
fkh6 is rescued by fkhUAS.cRa/Scer\GAL4odd-106
Expression of fkhScer\UAS.cRa from embryonic stage 10 under the control of Scer\GAL4odd-106 rescues the apoptosis and pathfinding defects seen in fkh6 mutant anterior dMP2 neurons.