RNaseZ^ED24/RNaseZ^ED24 individuals bearing 1 or two copies of either RNaseZ^HCM1.Tag:V5 or RNaseZ^HCM2.Tag:V5 show a decreased climbing ability, as compared to controls. Homozygotes bearing 1 copy of either RNaseZ^HCM1.Tag:V5 or RNaseZ^HCM2.Tag:V5 show a thickened heart wall at the larval and adult stages; homozygotes bearing 1 copy of RNaseZ^HCM1.Tag:V5 or RNaseZ^HCM2.Tag:V5 show increased end-systolic area in larval and adult hearts; homozygotes bearing 1 copy of RNaseZ^HCM2.Tag:V5 show increased end-diastolic area in larval hearts; homozygotes bearing 1 copy of RNaseZ^HCM1.Tag:V5 show decreased fractional shortening in the adult heart; homozygotes bearing 1 copy of RNaseZ^HCM2.Tag:V5 show decreased fractional shortening in the larval and adult heart. In homozygotes bearing 1 copy of RNaseZ^HCM1.Tag:V5 or RNaseZ^HCM2.Tag:V5, heart muscle cells show increased number of nuclei with increased ploidy.

JhI-1^ED24 homozygous mutants are larval lethal.

JhI-1^ED24 mutant somatic clones induced in JhI-1^{ΔMTS.T:SV5\V5} expressing background are significantly smaller than their twin spot clone in third instar larval eye discs and clones located posterior of the morphogenetic furrow where a band of cells synchronously enter the final round of mitosis show fewer cells in the S-phase and no cells in the M-phase of the mitotic cycle.

JhI-1^ED24;JhI-1^{ΔMTS.T:SV5\V5} mutant cells derived from JhI-1^ED24 homozygous mutant somatic clones induced in wing discs carrying the JhI-1^{ΔMTS.T:SV5\V5} transgene as well as a Minute mutation (to give the JhI-1^ED24 mutant clones a growth advantage) show a significant delay in the G[[2]]/M transition of the mitotic cell cycle compared to controls and a sharp increase in the production of reactive oxygen species (ROS) and DNA damage markers. However, no induction of apoptosis is observed in these clones either in the wing or the antenna imaginal discs. The JhI-1^ED24;JhI-1^{ΔMTS.T:SV5\V5} wing disc cells have normal size.

Homozygous JhI-1^ED24 or hemizygous JhI-1^ED24/Df(2R)12 embryos hatch into larvae at the same and size as heterozygous siblings. However, they do not live long as 80% of them dies soon after the first larval molt. The few animals that survive beyond 3 days after egg deposition do not grow and die within the next few days as undersized second instars.

Expression of JhI-1^hs.T:SV5\V5 by heat pulses delivered daily allows the rescue JhI-1^ED24 mutants to adulthood. The adult flies do not require any additional heat pulses for their survival. Both male and female escapers not expressing JhI-1^hs.T:SV5\V5 any longer show low fertility and in a few days after eclosion they become completely sterile. Resuming JhI-1^hs.T:SV5\V5 expression restores their fertility. After 8 days without JhI-1^hs.T:SV5\V5 expression, oogenesis in JhI-1^ED24 females stalls at stages 8-9. Extra-numeral germ-line cells are observed in mutant egg chambers. In contrast to wild-type egg chambers that display a single oocyte connected to 15 nurse cells surrounded by a layer of follicle cells, mutant egg chambers can have three oocytes and more than 40 nurse cells of different size. Some mutant egg chambers have the follicle cell layer completely missing or composed of significantly fewer cells. Several mutant cysts fuse as they bud off from the germarium. Upon dissection of mutant males, mutant testes is found thinner than those of control males. The middle section of mutant testes is reduced in diameter compared with controls. Mutant testes display several defects. Compared with wild-type, mutant testes show a reduction in the number of mitotically dividing gonialblasts at the apical tip. All post-meiotic germ cells (e.g. onion stage or elongated spermatids) are absent or underrepresented in the mutants. Compared with wild-type, mutant testes contain about half the number of cysts of individualising spermatids that appear as bundles of needle-shaped nucei. The most abundant cysts of mutant testes are those with sixteen fully-grown primary spermatocytes. These pre-meiotic cells contain a large nucleus with partially condensed chromosomes and misshapen Nebenkerns indicating a failure of meiosis.

Compared with polyploid wild-type cells, somatic clones of homozygous JhI-1^ED24 mutant fat body cell are small with small nuclei. The mutant cells display the same DNA replication pattern as cells in the twin spot.

One heat-shock treatment is sufficient to rescue early lethality and developmental arrest in JhI-1^ED24 mutants expressing JhI-1^hs.T:SV5\V5. The mutants undergo two larval molts and reach third instar but still fail to attain wild-type size and never pupariate. Instead, the keep crawling in the food for about ten days and then die. Wing discs dissected from the rescued larvae are smaller, but do not show elevated levels of cell death. The mutant cells display delayed cell cycle progression at the G2/M transition compared with wild-type.

Imaginal disc cells in somatic clones of homozygous JhI-1^ED24 show cell autonomous growth disadvantage. Clones induced early at the beginning of the first instar (96 h before dissection), no JhI-1^hs.T:SV5\V5 mutant cells are found, while large wild-type twin-spots are easily identifiable. When clones are induced later in development (60-70 h before dissection), each wild-type twin spot is accompanied by a JhI-1^ED24 mutant clone. However, mutant clones are substantially smaller than their wild-type twins.

RNaseZ^ED24 has increased mortality during development phenotype, suppressible by Hsap\ELAC2^hs.Tag:V5

RNaseZ^ED24 has decreased body size | third instar larval stage phenotype, suppressible by Hsap\ELAC2^hs.Tag:V5

RNaseZ^ED24 has decreased body weight | third instar larval stage phenotype, suppressible by Hsap\ELAC2^hs.Tag:V5

Hsap\ELAC2^hs.Tag:V5, RNaseZ^ED24 has abnormal developmental rate | larval stage phenotype

Hsap\ELAC2^hs.Tag:V5, RNaseZ^ED24 has some die during larval stage phenotype

Hsap\ELAC2^hs.Tag:V5, RNaseZ^ED24 has lethal - all die before end of pupal stage phenotype