Imprecise excision of the progenitor insertion, resulting in a deletion which removes all exons contributing to the open reading frame of the Mnt isoform that contains both the SID and bHLHZ domains.
Mutant flies show an increase n ommatidial size compared to controls.
The survival of homozygous and wild-type larvae under starvation conditions is not significantly different.
Homozygous embryos show no significant difference in hatching rates compared to controls. No defects are seen in larval molting, pupation or eclosion in homozygotes.
Mutant adult males are 20% heavier than wild-type controls. Mutant males have 18% fewer wing trichomes in a defined area of the adult wing, indicative of an increase in cell size.
Mutant females show a significant reduction in adult life span compared to controls. There is also a reduction in the maximal life expectancy (90% mortality) compared to controls.
Mnt1 is a suppressor of decreased body size | larval stage phenotype of Myc4
Mnt1, Myc4 has decreased body size | larval stage phenotype
Mnt1, Myc4 has decreased cell size | somatic clone phenotype
Mnt1 is a non-suppressor of ommatidium phenotype of MycUAS.cZa, Scer\GAL4GMR.PF
Mnt1, Myc4 has embryonic/larval fat body phenotype
Mnt1, Myc4 has wing disc | somatic clone phenotype
Mnt1, Myc4 has embryonic/larval salivary gland phenotype
The ability of dmΔMB2.αTub84B.T:HA1 to rescue the lethality of dm4 is increased if the flies are also mutant for Mnt1.
dm4 ; Mnt1 double mutant clones in the fat body contain tiny cells that have minuscule nuclei.
The eye phenotypes (apoptosis and increased ommatidial size) caused by expression of three copies of dmScer\UAS.cZa under the control of Scer\GAL4GMR.PF are not qualitatively altered by Mnt1/Y.