Nucleotide substitution: C?T.
Amino acid replacement: Q128term.
Nucleotide substitution: C659T. (Nucleotide numbering is according to cDNA clone RE27439).
C5464013T
C?T
Q128term | mid-PA; Q128term | mid-PB
Q128term
gonad | embryonic stage (with midB23)
mid1/mid8A69N1 embryos have disorganised and/or missing muscle fibers (lateral transverse muscles 3 and 4 and the segment border muscle).
mid1/mid1 embryos have a significantly reduced percentage presence of lateral transverse muscle 4 and a significantly increased number of nuclei in transverse muscle 4 compared to controls. In hemisegments with four LT muscles, mid1/mid1 embryos show a shift in fate of the LT4 muscle towards LT1-3: the most posterior LT muscle is no longer shifted dorsally and contains an increased number of nuclei compared to controls.
An additional, ectopic eve-postive neuron is observed within the nerve cord in 35-38% of hemisegments in ~14 hour-old mutant embryos. In midlos1/mid1 embryos, the ectopic neuron is seen in 30-39% of hemisegments; in mid2/mid1 embryos, the ectopic neuron is seen in 33-34% of hemisegments; in mid1/Df(2L)Exel6012 embryos, the ectopic neuron is seen in 63-66% of hemisegments. Further experiments suggest this is an ectopic RP2 (eRP2) neuron, resulting from the transformation of a wild type neuron termed the 'M-neuron', with an ectopic GMC-1-like cell and a RP2 sib-like cell also present. This extra RP2/sib lineage is formed 2-2.5 hours after the development of the bona fide RP2 lineage.
The longitudinal tracks are interrupted and the posterior commissures are thinner than normal in mid1 embryos.
The RP1 and RP3 motor axons stall or follow longitudinal axons in homozygous embryos (in wild-type embryos they exit the central nervous system towards the periphery).
Sensory axons in the peripheral nervous system branch excessively or cross segment borders in mutant embryos.
mid1 and mid1/Df(2L)x528 mutant embryos show a significant loss of NB1-1 in the odd-numbered abdominal segments (77.3% and 80% loss, respectively) while the loss of NB1-1 in the even-numbered abdominal segments is minimal (6.8 and 5%).
Stage 17 mid1 embryos show a partially penetrant heart phenotype, in which some embryos show defects in the alignment of cardioblasts and pericardial cells.
Stage 16 mid1 homozygous embryos have a normal number of cells in the dorsal vessel, which has normal overall morphology. But they have increased numbers of elongated, putative ostia forming cells per hemisegment in the heart region and a corresponding decrease in numbers of dorsal vessel cells expressing cardioblast markers.
Homozygous larvae show loss of denticles predominantly in the ventral-most region of odd-numbered segments.
Denticle bands are defective in the ventral midline.
mid1/mid1 is a suppressor of decreased cell number | embryonic stage phenotype of edlk06602
mid1/mid1 is a suppressor of embryonic heart ostial cardioblast phenotype of edlk06602
mid1/mid1 is a suppressor of heart primordium phenotype of edlk06602
mid1/mid[+] is a suppressor of chaeta | increased number phenotype of gcmPyx
Df(2L)BSC810, mid1 has segment border muscle cell phenotype
Df(2L)BSC810, mid1 has muscle cell of lateral oblique muscle 1 phenotype
Df(2L)BSC810, mid1 has embryonic/larval hypodermal muscle cell phenotype
Df(2L)BSC810, mid1 has muscle cell of lateral transverse muscle 4 phenotype
Df(2L)BSC810, mid1 has muscle cell of lateral transverse muscle 3 phenotype
mid1, ptc9 has ventral denticle belt phenotype
mid1/Df(2L)BSC810 embryos have disorganised and/or missing muscle fibers (lateral transverse muscles 3 and 4, segment border muscle, lateral oblique 1) compared to wild type.
mid1 is rescued by midUAS.cLa/Scer\GAL4Mef2.PR
mid1 is rescued by Scer\GAL4elav-C155/midUAS.cLa
midB23/mid1 is partially rescued by Scer\GAL4twi.PG/midUAS.cBa
midB23/mid1 is partially rescued by Scer\GAL4Six4.PT/midUAS.cBa
Driving midScer\UAS.cLa with Scer\GAL4Mef2.PR in mid1/mid1 embryos restores Kr expressing founder cells at the lateral transverse muscle 4 position.
Expression of midScer\UAS.cBa in the mesoderm under the control of Scer\GAL4twi.PG fully rescues the lack of somatic gonadal precursor (SGP) cluster fusion and germ cell ensheathment seen in midB23/mid1 mutant embryos. The number of scattered germ cells is reduced. The SGP-related defects are also rescued in the majority of embryos when midScer\UAS.cBa is expressed under the control of Scer\GAL4Six4.PT, but not to the extent seen with Scer\GAL4twi.PG.