Nucleotide substitution: C854T. Amino acid replacement: R185C.
C22069213T
C854T
R185C | how-PA; R185C | how-PB; R185C | how-PC; R185C | how-PD; R185C | how-PE; R185C | how-PF
R185C
howe44 germline clone mutant embryos exhibit an uneven distribution of mesoderm cells. In some regions the mesodermal cells migrate dorsally, while in others, the cells are retarded and do not reach the dorsal ectoderm domain. One or two segments lack cardiac and pericardial cells, or some of the dorsal muscle. These phenotypes indicate a defect in dorsal spreading.
Mutant embryos show defects in glial cell positioning. Peripheral glial cells do not migrate out of the central nervous system/peripheral nervous system (CNS/PNS) transition zone and accumulate at the nerve root. The cell body of the glial cell is found at the CNS/PNS transition zone and thin glial processes are sometimes seen along the intersegmental and segmental nerves. In some segments, glial cells have migrated along the nerve but do not fully differentiate and fail to enwrap the axon tracts. In some segments, the oenocytes are completely missing.
Close to the CNS/PNS transition zone, the perineurial glia does not fully wrap around the subperineurial glia in stage 16 mutant embryos. Further distal, glial cell processes are reduced in size leaving some axons in direct contact with the hemolymph.
About 50% of the embryos produced by howe44 germ-line clones show aberrant preblastoderm development that included unsynchronised nuclear divisions and cellularisation defects. The remaining 50% of the embryos complete cellularisation in a similar manner to that of wild-type embryos.
Homozygotes and hemizygotes die during late embryogenesis, with the most posterior end of the cuticle arrested above the dorsal surface. These embryos contain differentiated myoblasts, but show defects in myotube migration and attachment, resulting in disorganised and often round-shaped myotubes.
how alleles form the following allelic series (strongest to weakest): howe44, howr17, howx3, hows2612.