lethal (with Df(2L)ast2)
lethal (with Df(2L)BSC480)
lethal (with Df(2L)BSC521)
lethal (with Df(2L)dp-79b)
lethal (with Df(2L)ED7762)
lethal (with Df(2L)Exel6005)
larval mushroom body & neuroblast | somatic clone
testis | adult stage (with chinmoKG05386)
testis | adult stage (with chinmoST)
Arrested chinmo1/Df(2L)Exel6005 embryos appear short along the anterior-posterior axis.
chinmoM33/chinmo1, chinmo1/Df(2L)S2, chinmo1/Df(2L)ast2, chinmo1/Df(2L)dp-79b, chinmo1/Df(2L)Exel6005, chinmo1/Df(2L)ED7762, chinmo1/Df(2L)BSC480, or chinmo1/Df(2L)BSC521 mutants are lethal.
chinmo1/chinmo1 mutant somatic cyst stem cell clones are lost from the adult testis stem cell niche and testes do not exhibit any signs of sex transformation.
chinmoST/chinmo1 or chinmoKG05386/chinmo1 mutant males exhibit somatic cells with a follicle cell-like phenotype.
chinmo1 mushroom body neurons aberrantly acquire late-type neurite trajectories.
Few escapers with eye-antennal disc chinmo1 clones (in the Minute background) exhibit often only a rudimentary head when compared to controls.
At 2 days post-clone induction (pci), chinmo1 germline stem cell (GSC, Vasa staining) clones are in contact with the Hub (a group of somatic cells in testis) and cyst stem cell (CySC, Zfh1 or Tj staining) clones envelope germ line cells similar to control MARCM and flip-out clones. At 7 days pci, unlike controls, there isn't any CySc clones in contact with the Hub but there are Tj+ somatic clones outside of the Hub while there are numerous GSC clones in contact with the Hub similar to controls.
Knocking out chinmo using chinmo1 somatic clones in the GMC of the central complex sublineage causes the third sibling to exhibit a temporal cell fate similar to that of the fourth neuron in the wild-type lineage. Neurons derived from chinmo1 mutant third GMCs, as determined by associated wild-type neuroblast clones containing three cells, acquire projections that are characteristic of wild-type four siblings. They innvervate the middle subcompartment of the noduli with the wild-type sibling of the neuroblast clone. In addition, mutant third siblings, similar to wild-type fourth-born neurons, acquite a much more diffuse pattern of neurite elaboration in the lateral accessory lobe than wild-type third-born neurons.
chinmo1 mutant neuroblast clones, induced during production of the second GMC, do not produce detectable axons in the ventral subcompartment of the noduli.
Mushroom body neuroblast clones homozygous for chinmo1 generated at newly hatched larval stage contains only one vertical and one horizontal axon bundle despite presence of many cell bodies. Mutant neuroblast clones also contain ectopic bundles of axons that exhibit a high affinity for the mAb Fas2, suggesting that most of the axons in chinmo1 mutant neuroblasts likely differentiate as α/β type of mushroom body projections.
There appear to be far more projections of the pioneer α/β type in chinmo1 mutant neuroblast clones, with qualitatively fewer γ type neurons.
Many chinmo1 mutant mushroom body single cell clones, despite being derived during early larval development, aberrantly acquire late-type neurite trajectories. For example, following induction of mitotic recombination at two days after larval hatching, γ-type neurons are obtained in only one-third of the single-cell mushroom body clones (as oppose to 100% in wild-type), while many more single-cell mushroom body clones that have both vertical and horizontal projections, and that appear to be either α'/β' or pioneer α/β neurons, are obtained. Furthermore, only α'/β and pioneer α/β neurons are detected among the single-cell clones that are induced at three days after larval hatching.
chinmo1 heterozygous larvae exhibit α'/β' neurons in chinmo1 single-cell/two-cell clones induced at as early as three days after larval hatching and exhibit a higher percentage of α'/β neurons (approximately 45%) at the 3.25 day after larval hatching induction than the wild-type control (approximately 36%) at the 3.5 day after larval hatching induction. This indicates that, as compared to wild-type, α'/β' neurons are generated at least 0.25 days earlier in the chinmo1/+ heterozygous animals. In addition, pioneer α/β neurons are also born precociously in a chinmo1/+ heterozygous background, as evidenced by the phenomenon that 47% (compared to 4% in wild-type) of the single-cell/two-cell clones, induced within 12-6hr before pupal formation, develop into pioneer α/β neurons in chinmo1/+ heterozygotes.
Approximately 80 pioneer α/β neurons are present in chinmo1/+ adult flies, compared to an average of 60 in wild-type.
Labeled chinmo1 single-cell/two-cell clones, induced in newly hatched larvae, innervate the D, instead of DL1, glomeruli. They also exhibit an axon arborization pattern resembling that of wild-type D-targeting projection neurons. Thus, chinmo1 mutant projection neurons, born in newly hatched larvae, apparently develop into the D-targeting projection neurons that also belong to the anterodorsal lineage, but are normally not generated until about two days after larval hatching. In contrast, chinmo1 is dispensable for specification of late-born cell fates, with both chinmo1 mutant, and wild-type clones, sharing the same morphological features of late-born projection neurons: all clones elaborated dendrites in both DM6 and VA1lm glomeruli.
chinmo1 has abnormal neuroanatomy | somatic clone phenotype, non-enhanceable by lncRNA:let7CKO2
chinmo1 is a suppressor | partially of short lived phenotype of Df(2L)let-7-CGKI/lncRNA:let7CKO2, lncRNA:let7CΔmir-let7
chinmo1 is a suppressor | partially of abnormal locomotor behavior | adult stage | progressive phenotype of Df(2L)let-7-CGKI/lncRNA:let7CKO2, lncRNA:let7CΔmir-let7
chinmo1 is a suppressor of abnormal neuroanatomy | adult stage | progressive phenotype of Df(2L)let-7-CGKI/lncRNA:let7CKO2, lncRNA:let7CΔmir-125
chinmo1 is a suppressor | partially of short lived phenotype of Df(2L)let-7-CGKI/lncRNA:let7CKO2, lncRNA:let7CΔmir-125
chinmo1 is a suppressor | partially of abnormal locomotor behavior | adult stage | progressive phenotype of Df(2L)let-7-CGKI/lncRNA:let7CKO2, lncRNA:let7CΔmir-125
chinmo[+]/chinmo1 is a suppressor of abnormal neuroanatomy | dominant phenotype of lncRNA:let7CKO1
chinmo[+]/chinmo1 is a suppressor of abnormal neuroanatomy | dominant phenotype of lncRNA:let7CKO2
chinmo1 is a non-suppressor of abnormal neuroanatomy | adult stage | progressive phenotype of Df(2L)let-7-CGKI/lncRNA:let7CKO2, lncRNA:let7CΔmir-let7
chinmo1 has mushroom body | somatic clone phenotype, non-enhanceable by lncRNA:let7CKO2
chinmo1 has cyst progenitor cell | somatic clone | adult stage phenotype, non-suppressible by Scer\GAL4Tub.PU/BacA\p35UAS.cHa
chinmo1 has cyst progenitor cell | somatic clone | adult stage phenotype, non-suppressible by Scer\GAL4Tub.PU/zfh1UAS.cPa
chinmo1 is a suppressor of lipid droplet | adult stage phenotype of mir-125Δ.cSa
chinmo1 is a suppressor of adult fat body | adult stage phenotype of mir-125Δ.cSa
chinmo1 is a suppressor of adult brain phenotype of Df(2L)let-7-CGKI/lncRNA:let7CKO2, lncRNA:let7CΔmir-125
chinmo[+]/chinmo1 is a suppressor of mushroom body phenotype of lncRNA:let7CKO1
chinmo[+]/chinmo1 is a suppressor of mushroom body phenotype of lncRNA:let7CKO2
chinmo1 is a non-suppressor of adult brain phenotype of Df(2L)let-7-CGKI/lncRNA:let7CKO2, lncRNA:let7CΔmir-let7
The reduction in p.α/β mushroom body neurons in let-7-CKO1/+ or let-7-CKO2/+ adults is restored to normal numbers by chinmo1/+.
chinmo1; let-7-CKO2 double mutants neurons aberrantly acquire late-type neurite trajectories, as displayed by chinmo1 single mutant neurons. Mushroom bodies generated from double mutant neuroblasts appear identical to those generated from chinmo1 single mutants.
chinmo1 is rescued by chinmoUAS.fl/Scer\GAL4ey-OK107
Expression of chinmoScer\UAS.fl, under the control of Scer\GAL4OK107 grossly rescues the phenotypes characteristic of chinmo1 mutant mushroom body neuroblast clones.