A19161413T
A?G
K636term | ena-PA; K785term | ena-PB; K636term | ena-PC; K639term | ena-PD; K636term | ena-PE; K932term | ena-PF; K616term | ena-PG
N379F
An additional amino acid change at or near amino acid residue 379 is also observed in ena[23].
Nucleotide substitution: A?G.
Nucleotide substitution: A?T.
Amino acid replacement: N379F.
Amino acid replacement: K636term.
actin filament & egg chamber | germ-line clone
follicle cell & actin filament | somatic clone
ena23 zygotic/maternal mutant embryos display a wavy leading edge during dorsal closure, with defects in leading edge cell shape, a reduced rate of zippering and deep and persistent segmental grooves.
Approximately 90% of ena23 zygotic mutants exhibit virtually wild-type cuticles, whereas 8% display head holes.
24% of eggs derived from females carrying homozygous germline clones show a "dumpless" phenotype.
Egg chambers in females with homozygous germline clones have defects in the cytoplasmic filaments (the bundled cytoplasmic actin filaments extending from the cortex to nuclei). No defects in ring canal formation or growth are seen in mutant egg chambers. Some egg chambers contain multinucleate nurse cells.
Homozygous follicle cell clones do not usually cause significant disruptions in either epithelial organisation or in the assembly of cortical actin into follicle cells adherens junctions in stage 2-7 egg chambers. However, in later egg chambers, clones with reduced cortical actin and disruptions in epithelial integrity are seen.
Leading edge cells in embryos that are maternally and zygotically mutant for ena show a large decrease in average lamellipodial area and a striking decrease in filopodial number.
Homozygous clones that encompass the morphogenetic furrow do not result in a defect in cell constriction in the morphogenetic furrow.
ena23/enaGC1 embryos have reduced longitudinal axons in the central nervous system.
74% of zygotic ena23 mutant embryos have a wild-type cuticle, while 21% show misalignment/puckering along the dorsal midline.
Mature embryos that are both maternally and zygotically mutant for ena (ena23/enaGC1 embryos derived from females with homozygous ena23 germlines) proceed through gastrulation normally and have normal epithelial integrity. Segmental grooves are deeper than normal in these embryos and persist long after they should have regressed. The leading edge during dorsal closure is often uneven. Most of the embryos fail in head involution. Cells that should lead head involution appear to constrict far more than in wild type, nearly severing the head from the thorax.
Mature embryos that are both maternally and zygotically mutant for ena (ena23/enaGC1 embryos derived from females with homozygous ena23 germlines) show defects in the cuticle; 10% have a dorsal pucker, 37% have a hole in the head, 15% have both a dorsal pucker and a hole in the head and 28% have a large ventral hole.
Single cell γ neuron mutant clones in the mushroom body show drastic axon growth defects.
Homozygous embryos do not show midline crossing errors by axons in the central nervous system.
Mutant follicle cell clones lose cortical actin filaments from apical, basal and lateral sites.
96% of ISNb axons show a bypass phenotype in homozygous embryos.
Lethal in combination with enaGC1.
ena23 has abnormal cell shape phenotype, enhanceable by pyd[+]/pydB12
ena23 has abnormal cell shape phenotype, enhanceable by pydex180/pyd[+]
ena23 has abnormal cell shape phenotype, enhanceable by cnoR2/cno[+]
ena23/ena[+] is an enhancer of abnormal cell shape phenotype of cnoR2
ena23/ena[+] is a suppressor of visible | adult stage phenotype of Hsap\ABL1::Hsap\BCRUAS.cBa, Scer\GAL4GMR.PU
ena23/ena[+] is a suppressor of abnormal cell migration phenotype of CskGD9345, Scer\GAL4ptc-559.1
ena23/ena[+] is a suppressor of abnormal cell migration phenotype of Rho1UAS.cMa, Scer\GAL4ptc-559.1
ena23/ena[+] is a suppressor of abnormal cell migration phenotype of Scer\GAL4ptc-559.1, hepUAS.cUa
ena23/ena[+] is a suppressor of abnormal neuroanatomy phenotype of DAAMC.UASp/DAAMC.Scer\UAS.P\T
ena23/ena[+] is a non-suppressor of abnormal neuroanatomy | semidominant | embryonic stage phenotype of mir-8Δ
ena23 has embryo | dorsal closure stage phenotype, enhanceable by pyd[+]/pydB12
ena23 has embryonic leading edge cell phenotype, enhanceable by pyd[+]/pydB12
ena23 has ventral head epidermis phenotype, enhanceable by pyd[+]/pydB12
ena23 has embryonic head phenotype, enhanceable by pyd[+]/pydB12
ena23 has embryo | dorsal closure stage phenotype, enhanceable by pydex180/pyd[+]
ena23 has embryonic leading edge cell phenotype, enhanceable by pydex180/pyd[+]
ena23 has ventral head epidermis phenotype, enhanceable by pydex180/pyd[+]
ena23 has embryonic head phenotype, enhanceable by pydex180/pyd[+]
ena23 has embryo | dorsal closure stage phenotype, enhanceable by cnoR2/cno[+]
ena23 has embryonic leading edge cell phenotype, enhanceable by cnoR2/cno[+]
ena23 has ventral head epidermis phenotype, enhanceable by cnoR2/cno[+]
ena23 has embryonic head phenotype, enhanceable by cnoR2/cno[+]
Atg9B5, ena23 has nurse cell phenotype, suppressible by Atg9Tag:HA
ena23/ena[+] is an enhancer of nurse cell phenotype of Atg9B5
ena23, chic[+], ena[+], chic221 is an enhancer of nurse cell phenotype of Atg9B5
ena23/ena[+] is an enhancer of embryo | dorsal closure stage phenotype of cnoR2
ena23/ena[+] is an enhancer of embryonic leading edge cell phenotype of cnoR2
ena23/ena[+] is an enhancer of ventral head epidermis phenotype of cnoR2
ena23/ena[+] is an enhancer of embryonic head phenotype of cnoR2
ena23/ena[+] is an enhancer of embryo | dorsal closure stage phenotype of pydB12
ena23/ena[+] is an enhancer of embryonic leading edge cell phenotype of pydB12
ena23/ena[+] is an enhancer of ventral head epidermis phenotype of pydB12
ena23/ena[+] is an enhancer of embryonic head phenotype of pydB12
ena23/ena[+] is an enhancer of embryo | dorsal closure stage phenotype of pydex180
ena23/ena[+] is an enhancer of embryonic leading edge cell phenotype of pydex180
ena23/ena[+] is an enhancer of ventral head epidermis phenotype of pydex180
ena23/ena[+] is an enhancer of embryonic head phenotype of pydex180
ena23/ena[+] is a suppressor of eye phenotype of Hsap\ABL1::Hsap\BCRUAS.cBa, Scer\GAL4GMR.PU
ena23/ena[+] is a suppressor of wing disc phenotype of CskGD9345, Scer\GAL4ptc-559.1
ena23/ena[+] is a suppressor of wing disc phenotype of Rho1UAS.cMa, Scer\GAL4ptc-559.1
ena23/ena[+] is a suppressor of wing disc phenotype of Scer\GAL4ptc-559.1, hepUAS.cUa
ena23/ena[+] is a suppressor of neuropil | embryonic stage phenotype of DAAMC.UASp/DAAMC.Scer\UAS.P\T, Scer\GAL4elav-C155
ena23/ena[+] is a suppressor of fascicle | embryonic stage phenotype of DAAMC.UASp/DAAMC.Scer\UAS.P\T, Scer\GAL4elav-C155
ena23/ena[+] is a suppressor of symmetrical commissure | embryonic stage phenotype of DAAMC.UASp/DAAMC.Scer\UAS.P\T, Scer\GAL4elav-C155
ena23/ena[+] is a non-suppressor of larval intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype of mir-8Δ
ena23/ena[+] is a non-suppressor of axon | embryonic stage phenotype of mir-8Δ
Atg9B5, chic[+]/chic221, ena23/ena[+] has nurse cell ring canal | decreased number phenotype
Arpc11, ena23/ena[+] has filopodium phenotype
chic221, ena23/ena[+] has filopodium phenotype
chic05205a, ena23/ena[+] has filopodium phenotype
DAAMEx68, ena23/ena[+] has filopodium phenotype
An ena23 heterozygous mutant background suppresses the actin remodelling and subsequent basolateral invasion of epithelial cells seen in flies expressing CskGD9345 in a stripe of cells at the anterior/posterior boundary of the larval wing disc under the control of Scer\GAL4ptc-559.1.
An ena23/+ background suppresses the cell migration seen upon expression of Rho1Scer\UAS.cMa under the control of Scer\GAL4ptc-559.1.
An ena23/+ background suppresses the cell migration seen upon expression of hepScer\UAS.cUa under the control of Scer\GAL4ptc-559.1.
ena23 is unable to suppress the fertility defects seen in Df(1)NetABΔ. The courtship behaviour defects seen in Df(1)NetABΔ mutant males are also not rescued.
Reducing pyd levels, through a pydB12 or pydex180 heterozygous background, strongly enhances the morphogenesis defects found in zygotic ena23 mutants, substantially increasing the frequency of failure of head involution.
Reducing ena levels, through an ena23 heterozygous background, substantially enhances the severity of the pydB12 or pydex180 zygotic/maternal phenotype; more than one-third of the mutants exhibit large holes in the cuticle, suggesting disruption of epithelial integrity.
An ena23 heterozygous background enhances the cnoR2 zygotic phenotype, with 38% of progeny exhibiting head and/or dorsal holes, and 4% displaying a novel, stronger phenotype in which only the ventral cuticle remains.
Reducing maternal and zygotic cnoR2 levels strongly enhances the ena23 zygotic phenotype, with 50% of the progeny exhibiting head holes.
Cultured primary neurons derived from ena23/+ Sop21/+ and DAAMEx68/+ ena23/+ double heterozygous embryos show a significant reduction in the number of filopodia compared to control neurons.
Cultured primary neurons derived from chic221/+ ena23/+ and chic05205a/+ ena23/+ double heterozygous embryos show a significant reduction in the number of filopodia compared to control neurons.
The Scer\GAL4elav-C155/DAAMC.Scer\UAS.P\T gain-of-function phenotype (i.e the appearance of thicker commissures and nerve roots) is suppressed by a ena23/+ background.