Truncated Chro612 protein is missing parts of the COOH-terminal domain important for spindle localisation.
EMS-generated point mutation in Chro that introduces a premature stop codon resulting in a truncated 612 amino acid protein that retains the chromodomain.
Nucleotide substitution: C2024T
The central brain neuroblast reactivation defects (manifested by the retention of cellular extensions and low mitotic activity even at late larval stages) characteristic for Chro71/Chro612 mutants are alleviated by expression of grhScer\UAS.cUa under the control of Scer\GAL4insc-Mz1407 in the mutant background or by combination with a single copy of pros17, the phenotype can be further improved when both grhScer\UAS.cUa expression as well as the pros17 heterozygosity are combined.
Expression of ChroScer\UAS.P\T.FL.T:Ivir\HA1,T:Zzzz\FLAG,T:Avic\GFP in third larval instar salivary glands rescues all aspects of polytene chromosome morphology in Chro71/Chro612 animals.
Expression of ChroNTD.Scer\UAS.P\T.T:Avic\GFP.T:SV40\nls2 in third larval instar salivary glands substantially rescues polytene chromosome morphology in Chro71/Chro612 animals, although some regions of the chromosome arms remain coiled.
Expression of either ChroNTD-ΔChD.Scer\UAS.T:Uuuu\nls6,T:SV5\V5 or ChroChD.Scer\UAS.T:SV40\nls2,T:SV5\V5,T:Avic\GFP in third larval instar salivary glands results in no or very little improvement of polytene chromosome morphology in Chro71/Chro612 animals.