Polytene chromosomes normal.
7kb insertion of middle repetitive DNA element located 5' to the en transcript.
Construct: Nucleotide substitution: C2236A. 3' untranslated region carries insertion of bases TA at nucleotide position 2015 and nucleotide substitution C2236A.
7 kb insert at 0 kb
wing & macrochaeta
Homozygotes exhibit a variety of wing vein alterations in the posterior compartment of the wing. Transheterozygotes with enEnci have a posterior specific wing phenotype: bristles characteristic of the anterior wing margin are present on the posterior wing margin. Males have duplicated sex combs on the prothoracic legs.
Mutation has no effect on the hhMrt phenotype.
Viable.
Coordinate mutant.
Additional bristles in the second leg.
Homozygous adults have abnormal wings, with a posterior to anterior transformation. The sex comb on the male prothoracic leg is partially duplicated posteriorly. The posterior wing is grossly disrupted in en1/en2 transheterozygotes, rarely having an organised fourth or fifth vein. The sex comb on the male prothoracic leg is duplicated posteriorly, more distal leg segments are fused and terminal claws are sometimes missing. The arista and other anterior elements of the antenna are often duplicated.
The posterior wing is an abnormal shape in homozygous flies. The posterior wing veins have a variable disrupted pattern, with the anterior crossvein (ACV) often being absent or reduced and vein III often appearing slightly thickened. The campaniform sensillum associated with the ACV is often absent, while the campaniform sensilla of vein III may be increased in number. Campaniform sensilla are often found in the posterior wing, where they may or may not be associated with vein tissue. Many posterior margin hairs are transformed into socketed bristles, some of which are similar to the thick middle row bristles of the anterior margin. Parts of the posterior margin are thickened into vein tissue similar to the anterior margin in some wings. The alar lobe carries socketed bristles. There is a cleft in the scutellum. Approximately five irregularly arranged "secondary" sex-comb teeth are found on the posterior tarsus of the foreleg. en1/Df(2R)en-A or en1/Df(2R)en-B hemizygotes are sterile. They have a less distorted posterior wing blade than en1 homozygotes. The posterior wing venation varies from wild-type in occasional cases to severely disrupted. The posterior margin is never thickened to form vein tissue, and carries fewer socketed bristles than en1 homozygotes. These bristles tend to look like double row or dorsal or ventral triple row bristles. The alar lobe is wild-type. The scutellum is broader than wild-type and sometimes shows an incipient cleft. en57/en1, en10/en1, en54/en1 or en58/en1 flies have wild-type shape wings and a wild-type scutellum. Vein III appears thickened and tends to have a posteriorwards bulge about halfway along its length. The anterior crossvein (ACV) is often reduced or absent. Small plexae of vein tissue tend to occur close to the ACV and the posterior crossvein. Vein IV is frequently interrupted and often carries campaniform sensilla. Bristles are occasionally seen in the posterior row, but they never have the characteristics of the middle triple row.
Severe thoracic morphological defects.
Male en1 homozygotes have abnormal genitalia, with a reduction in the number of clasper teeth, rudimentary dorsal parameres of the penis apparatus, and often incomplete rotation of the penis apparatus. Viable heteroallelic combinations with other en alleles show a more extreme phenotype, with a reduction in the genital arch process, hypandrium and hypandrial phragma as well. Extra genital arch and anal plate bristles are sometimes seen. Female flies carrying en1 and another en mutation show variable genital abnormalities, ranging from no abnormalities, to reduced dorsal and ventral vaginal plates, which sometimes have a giant bristle. Extra bristles and pigmentation are sometimes seen on the eighth tergite.
At 29oC the third segment of the antenna is larger than wild-type in homozygous flies, and a bristle close to the border is often enlarged. This phenotype is enhanced by the M(3)65F mutation. en1/en2 transheterozygotes have abnormal antennae, the phenotype increasing at higher temperatures (25 or 29oC). At 29oC the posterior compartment of the second segment is almost always abnormal, having extra anterior-like bristles which are often arranged in a mirror-image symmetry with respect to the anterior compartment. The third segment is usually larger than normal and is often bilobed. Approximately half the antennae having a bilobed third segment also have an extra arista. en1/en2 transheterozygotes also have abnormal wings; at 17oC they are grossly enlarged, there is scalloping of the posterior margin, and the triple rows of anterior-like bristles are poorly formed. At 29oC the wings are not enlarged and a well-formed triple row develops on the posterior margin.
Homozygous clones in the wing are frequently lost in the posterior but not the anterior compartment.
Duplications of transverse rows in female prothoracic leg, extra bristles in mesothoracic and metathoracic tarsi.
In males, extra sex comb often present smaller than normal and in mirror-image position in posterior compartment.
viable
en1, ph-plac has wing vein L4 phenotype
en1/en54, ph-plac has wing vein L4 phenotype
cg1, en1 has wing vein L4 phenotype
In Pka-R2Cos-A1, en1 double mutants the duplications characteristic of Pka-R2Cos-A1 only occur in the original anterior compartment, and not in the transformed posterior compartment, indicating that the Pka-R2Cos-A1 duplications develop as a position response.
Evang, 7th Nov. 1926.
Eker.
Action of en1 is autonomous except for in the scutellar cleft.
Clonal analysis shows that en function is required only in the posterior compartment in the antenna.
Examination of gap-junction mediated exchange of small fluorescent molecules in en- wing discs reveals a boundary of restricted communication that appears to be identical to the wild-type A-P communication restriction boundary.
The loss of function phenotype of en1 may be explained by the partial redundancy of function of inv.
en mutants can be ranked by strength regarding their ability to induce a ci phenotype: en1 <= Df(2R)en30 <= en4 <= enEnci <= Df(2R)en-SFX31 <= en59.