The oviduct muscle of Col4a1^DTS-L3 homoygotes loses the typical sarcomeric structure at the restrictive temperature of 29[o]C, but not at the permissive temperature of 20[o]C; there are areas of actin bundling that extend beyond the area of a regular sarcomere; the Z-disc structure is disrupted; muscle fiber diameters decrease and become more heterogeneous.

At restrictive temperature (29[o]C), Cg25C^DTS-L3/Cg25C^DTS-L3 mutant epithelial cells develop actin stress fibers (visible after 3 days incubation, abundant after 18 days); integrin and actin connections appear disrupted.

Third instar Cg25C^DTS-L3 larvae are shorter in length at 29[o]C compared to at 20[o]C and wild type larvae (at either temperature). At either temperature mutant larvae have shorter guts compared to wild type. At 29[o]C mutant midguts are enlarged, with several diverticula; areas of diverticula lack cellular organization and have protruding peritrophic matrix, and most nuclei within diverticula show signs of DNA fragmentation. At 20[o]C, intestinal dysfunction occurs at a similar time (after 57 days) in both wild type and mutant flies; at 29[o]C, Cg25C^DTS-L3 flies show intestinal dysfunction much earlier (20-22 days) than wild type.

The number of colony forming units of gut microbial flora in wild type significantly decreases at 29[o]C compared to 20[o]C, unlike in Cg25C^DTS-L3 larvae (show a non-significant reduction); mutants also show a shift toward Acetobacter cerevisiae in Acetobacter cerevisiae/Lactobacillus plantarum gut ratios (at either 20 or 29[o]C). Cg25C^DTS-L3 flies reared at 29[o]C have a significantly shorter lifespan compared to wild type flies; oral feeding of Acetobacter cerevisiae or Lactobacillus plantarum at 29[o] decreases lifespan similarly in mutants and wild type flies.

Cg25C^DTS-L3 embryos show an alary muscle detachment phenotype. Alary muscle detachment in Df(2L)Exel7022 transheterozygous embryos is more penetrant at higher temperatures.

Cg25C^DTS-L3/Cg25C^S3064 is embryonic lethal at 25[o]C, but if kept at 19[o]C some animals develop into early L1 larvae.

Adult escapers are observed if combined with Cg25C^S0791 or Cg25C^S1348 or Cg25C^S2186 and grown at 19[o]C, while at 25[o]C these trans-heterozygotes die either during larval growth or in pupal stages.

Cg25C^DTS-L3 heterozygotes show dominant semi-lethality at 29[o]C but are viable at 20[o]C. Homozygotes raised at 20[o]C are lethal.

Oviductal myofibers in heterozygous Cg25C^DTS-L3 mutant flies detach laterally from each other with focal splitting of the basement membrane at both the restrictive (29[o]C) and permissive (20[o]C) temperature. Even at the permissive temperature myofibers are partially rounded up at their otherwise spiky ends, the nuclei are centrally located and F-actin is diminished in the peri-nuclear space. At the restrictive temperature, loss of F-actin extends to large areas of the sarcoplasm. Myofibers with loose lateral contact are prominently rounded and the nuclei are central with condensed chromatin. The basement membrane surrounding the myofibers appears distorted, thinned or absent.

Heterozygous Cg25C^DTS-L3 mutants exhibit a gradually developing female sterility at the restrictive temperature (29[o]C).

Heterozygous Cg25C^DTS-L3 mutants raised at the restrictive temperature (29[o]C) stop active crawling and eager pursuit of food at the third instar larval stage.

Electron microscope analysis of heterozygous Cg25C^DTS-L3 mutant oviduct muscle sarcomeres shows that they lack precise transverse alignment and comprise dense Z and A bands and wide I bands. These phenotypes are seen at both the permissive and the restrictive temperature. At the restrictive temperature, only Z bands can be recognised, the A and I bands are not separated, and degradation of muscle fibers appears as electron-lucent areas between persisting Z bands.

Col4a1^DTS-L3 has lethal | recessive phenotype, suppressible by vkg^k16721

Col4a1^DTS-L3 has lethal | recessive phenotype, suppressible by vkg^hsneo80

Col4a1^DTS-L3 has lethal | recessive phenotype, suppressible by vkg^sz-78

Col4a1^DTS-L3 has lethal | recessive phenotype, suppressible by vkg^b-35

Col4a1^DTS-L3 has lethal | recessive phenotype, suppressible by vkg^b-14

Col4a1^DTS-L3 has lethal | recessive phenotype, suppressible by vkg^sz-14

Col4a1^DTS-L3 has lethal | recessive phenotype, suppressible by vkg^sz-6

Col4a1^DTS-L3 is a suppressor | partially of lethal | recessive phenotype of vkg^hsneo80

Col4a1^DTS-L3 is a suppressor of lethal | recessive phenotype of vkg^k16721

Col4a1^DTS-L3 is a suppressor of lethal | recessive phenotype of vkg^sz-14

Col4a1^DTS-L3 is a suppressor of lethal | recessive phenotype of vkg^sz-78

Col4a1^DTS-L3 is a suppressor of lethal | recessive phenotype of vkg^sz-6

Col4a1^DTS-L3 is a suppressor of lethal | recessive phenotype of vkg^b-14

Col4a1^DTS-L3 is a suppressor of lethal | recessive phenotype of vkg^b-35