|Feature type||allele||Associated gene||Dmel\how|
|Also Known As||howstru|
What does this section display?
This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms).
What does this section not display?
This section does not currently display links that were removed or gene model changes.
Click the icon below to subscribe to this FlyBase record and receive updates automatically through your feed reader.
|All updates||Click here to see a list of all updates to this record from FB2010_08 and on.|
|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
|Phenotype Manifest In|
Two days after clone induction, how[stru-3R-3] germline stem cells are observed in 38% of testes (compared to control clones being found in 68% of testes). how[stru-3R-3] homozygous germline stem cell clones are completely lost in 5-8 days after clone induction. Germline stem cells lacking how function do not differentiate prematurely into spermatogonia. The morphology of how[stru-3R-3] homozygous mutant two-cell cysts is abnormal; in particular how[stru-3R-3] mutant cells are larger than surrounding wild-type spermatogonia of the equivalent stage. how[stru-3R-3] mutant germline stem cell and spermatogonia clones are larger in size than their wild-type counterparts. Fusomes that connect how[stru-3R-3] sibling cells are larger than comparable wild-type cells. Consistent with their larger size, how[stru-3R-3] mutant spermatogonia contain larger nucleoli than their wild-type counterparts. how[stru-3R-3] mutant spermatogonia contain the correct number of centromeres. In addition, very few of these cells are observed to incorporate BrdU, indicating that they are not endoreplicating. how[stru-3R-3] mutant germline stem cells exhibit a delay in the G2 phase of the cell cycle due to a lack of CycB and are eliminated from the germline via apoptosis.
Pre-blastoderm development is normal. A delay in mesoderm invagination is seen in zygotic mutant embryos. About 50% of homozygous mutants show defective mesoderm invagination. In most mutant embryos invagination does eventually take place, but is not synchronous; the delamination of the mesoderm cells from the ectoderm is sporadic compared to wild-type. A significantly higher number of mitotic nuclei are seen than in wild-type. Dividing cells are seen in the mesoderm anlage which is mitotically silent in wild-type. No difference is seen in developmental rate between wild-type and mutant embryos.
Mutants show an increased number of tendon cells at late stages of embryonic development (after muscle binding has occurred) compared to wild type.
Homozygous clones in the wing produce discrete, round blisters of variable size. These blisters can be located anywhere on the wing. Wing venation is normal.
Homozygous clones in the wing produce a blistered phenotype.
|Phenotype Manifest In|
A how[stru-3R-3] heterozygous background results in the generation of 8-cell cysts of spermatocytes and suppresses the extra divisions present in bam[Δ86]/+ males.
|Complementation & Rescue Data|
|Fails to complement|
|Stocks ( 1 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 5 )|
|Secondary FlyBase IDs|
|References ( 13 )|
|Personal communication to FlyBase|