Amino acid replacement: V353M.
G10326481A
V353M | RnrL-PA
V353M
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
Homozygous RnrLA4B5 mutant eyes show strong defects in compensatory growth in response to tissue loss (induced by generating larval clones of the temperature-sensitive cell-lethal mutation sec5ts1 under the control of Scer\GAL4en-e16E at the restrictive temperature). The resulting eyes are smaller than wild type. No defects in cell proliferation are detected when the sec5ts1 cells are not ablated (i.e. when the flies are maintained at the permissive temperature). The proportion of mutant eye tissue seen following generation of wild type non-ablating clones is similar at 25[o]C and 30[o]C suggesting the mutation is not temperature sensitive. No compensatory growth defects are seen in RnrLA4B5 mutant eyes when tissue is ablated during the larval stages using irradiation.
Homozygous RnrLA4B5 mutant wings are small and exhibit substantial defects following tissue loss (induced by generating homozygous mutant wing disc clones of the temperature-sensitive cell-lethal mutation sec5ts1 at the restrictive temperature). At 48 hours after the shift to the restrictive temperature the wing discs are similar in size to controls, however the posterior compartment shows very high levels of apoptotic cells. Despite this, mitotic cell are also seen.
Homozygous RnrLA4B5 mutant wing disc clones are indistinguishable from controls.
RnrLA4B5 is a suppressor of increased cell number | somatic clone phenotype of ykiS168A.UAS.EGFP,Tag:HA
RnrLA4B5 is a suppressor of wing disc | somatic clone phenotype of ykiS168A.UAS.EGFP,Tag:HA
Homozygous RnrLA4B5 partially suppresses the wing disc overgrowth phenotype seen when ykiS168A.Scer\UAS.T:Avic\GFP-EGFP,T:Ivir\HA1 mutant clones are generated under the control of Scer\GAL4αTub84B.PL.