DNA sequencing failed to identify any point mutations in the sequence coding for qless-PA.
Post-embryonic generation of qless109 MARCM clones in the optic lobe, central brain or thoracic neuromeres results in dramatic reduction in neuroblast clonal growth by 96 hours after larval hatching. Whereas a single large mira[+] neuroblast is observed in each wild type clone, this cell type is missing in the majority of thoracic qless109 clones. There is also a large reduction in postmitotic progeny - qless109 clones in the central brain or thoracic neuromeres contain only ~20% or ~14%, respectively, of the wild type number of cells per clone.
Dietary supplementation of with Coenzyme Q with side-chain length of 10, 9 or 4 isoprenoid units rescues the presence of a mira[+] neuroblast and the number of cells per clone in qless264 MARCM clones to near wild type levels in both the central brain and thoracic neuromeres.
Most neurons in qless264 MARCM clones at 96 hours after larval hatching are undergoing caspase-mediated apoptosis. qless264 cells also experience increased mitochondrial stress, as judged by Hsp60 upregulation.
qless264 has abnormal neuroanatomy | somatic clone | larval stage phenotype, suppressible by Scer\GAL4unspecified/BacA\p35UAS.cHa
qless264 has abnormal stress response | somatic clone | larval stage phenotype, non-suppressible by Scer\GAL4unspecified/BacA\p35UAS.cHa
qless264 has larval neuroblast | somatic clone phenotype, suppressible by Scer\GAL4unspecified/BacA\p35UAS.cHa
Expression of BacA\p35Scer\UAS.cHa within qless264 MARCM clones does not prevent mitochondrial stress, but does efficiently rescue the number of cells per qless264 clone.