Gene expression is increased in response to the presence of either one or two copies of Scer\GAL4^hs.PB.

dsRNA made from templates generated with primers directed against this gene is tested in an RNAi screen for effects on actin-based lamella formation.

An ovo protein binding site near the otu transcription start site is required for ovo-dependent otu transcription in vivo.

otu is required during pupal and adult stages for the cystocyte divisions that give rise to the egg chamber. otu may also have a role in other oogenic functions.

otu is required for the organisation of actin filaments during multiple stages of oogenesis.

Female germ cells do not require otu function for survival before pupariation.

Variation of a microsatellite within the otu locus has been studied in North American populations of D.melanogaster.

The pseudonurse cells of otu mutants give rise to polytene chromosomes. Nurse cell-specific genes are functional in the pseudonurse cells, but the transport of pum, otu, ovo and bcd RNAs to the cytoplasm is affected. The nuclear localisation of otu and pum mRNA correlates with chromosome polytenisation.

otu and ovo are required cell autonomously in the female germline for germ cell proliferation and differentiation. XY germ cells do not require otu when developing in testes, but become dependent on otu function for proliferation when placed in an ovary. The requirement for ovo is dependent on a cell autonomous signal derived from the X:A ratio. The differential regulation of the otu and ovo genes provides a mechanism for the female germline to incorporate both somatic and cell-autonomous inputs required for oogenesis.

Alleles of otu can partially enhance the mutant phenotype of ovo^D2/+ heterozygous ovaries.

Examination of embryonic gonads indicates that reduction in zygotic otu activity sufficient to cause agametic adult ovaries does not affect the proliferation or viability of the embryonic germline. Pupal gonads fail to produce egg chambers indicating that the agametic adult phenotype is caused by a block in oogenesis before cyst formation, rather than the degeneration of existing egg chambers. otu function is not essential for germline viability before pupariation but is required in the pupal and adult ovaries. otu activity is limited to prepupal stages is not sufficient to support oogenesis, induction during pupal and adult stages causes suppression of the otu mutant phenotype.

The 104kD isoform of otu is required for normal proliferation of female germline cells and perhaps for oocyte differentiation. The 98kD isoform appears to be dispensible but can provide an otu function needed for the completion of oocyte maturation.

ovo, otu, snf and Sxl are not involved in the early events of germline sex determination, but are required later, during metamorphosis or in the adult for oogenesis.

Tumorous cells produced by otu mutants are capable of female-specific transcription and RNA processing indicating the ovarian cells retain some female identity. It is proposed that mutations do not cause male transformation of the female germ line but instead either cause an ambiguous sexual identity or block specific stages of oogenesis.

The 98kD isoform of otu is sufficient to allow proliferation of female germ cells during early oogenesis and is also involved in later stages of oogenesis. The 104kD isoform of otu is required for the differentiation of nurse cell and oocytes by some mechanism that involves Sxl. The 98kD isoform differs from the 104kD isoform in that it appears to act independently of Sxl.

Mutants display germline hyperplastic phenotype.

Partial germline sex transformation occurs in otu, snf, Sxl and bam ovarian tumors.

Phenotypic complexity of otu mutant ovaries is due to a dosage-dependent requirement for otu activity.

Reciprocal cross and expression analysis suggest a maternal requirement for otu⁺ in the development of the female germline.

The genetic hierarchy regulating female germ-line sex determination includes tra, tra2, dsx, fu, otu, ovo, snf and Sxl. otu⁺, ovo⁺ and snf⁺ activities are required for female-specific Sxl⁺ pre-mRNA splicing within 2X germ-line cells.

Mutant germ cells in otu ovaries have a morphology similar to primary spermatocytes and express male-specific reporter genes and have male-type Sxl splicing.

otu acts upstream of Sxl in germline sex determination. Gene dosage studies demonstrate additional interaction with mutations at the ovo locus.

Molecular analysis of otu locus and alleles reveals that the absence of otu function produces the most severe QUI class of phenotype (i.e. produce ovarioles lacking in germ cells), while the ONC mutants ( which produce cystocytes that continue dividing and form tumors) express lower levels of otu than those of the DIF class (which produce chambers containing only 'pseudonurse' cells).

otu gene product performs several functions during oogenesis.

Effects of otu mutations on male fertility were studied: there is a strong correlation between male sterility and severity of impairment in the female phenotype. Spermatogenesis is apparently normal, and male sterility was shown to be a consequence of failure in mating behaviour where wild type females refuse to react to the courtship attempts of mutant males.

The banding pattern of pseudonurse cell polytenes is similar to that of the polytenes from larval salivary gland cells.

Most cystocytes undergo complete cytokinesis and there are defects in the construction and functioning of the polyfusomal system during the cycles of cystocyte divisions.

Mutant nurse cells that fail to pump their cytoplasm into the oocytes are also unable to form a system of actin microfilament bundles in their cortical cytoplasm during stage 10B.

The 3' ends of Cp36 and otu map within 5kb of each other.

otu is required for establishment of ovarian germ cells, for correct division of the germ cells and for normal development within the 15 nurse cell-oocyte syncytium.

Oocyte differentiation is destabilized in certain otu alleles.

Homozygous females are defective in proliferation, differentiation, or maturation of the germ line, depending on the level of activity of the particular allele. So-called quiescent alleles (QUI) produce ovarioles lacking in germ cells; oncogenic alleles (ONC) produce cystocytes that continue dividing and form tumors; differentiated alleles (DIF) produce chambers containing only 'pseudonurse' cells (PNCs) or nurse cell/oocyte (NC/O) syncytia. In these, transport of nurse cell cytoplasm to the oocyte is inhibited and chambers are arrested at a pseudo-12 stage.

Drosophila nurse cells normally undergo nine or ten cycles of DNA replication and the chromatids dissociate so that each nucleus is filled with a jumbled mass of oligotene threads. In otu pseudonurse cells, the chromatids remain in register, generating banded polytene chromosomes. The largest polytenes have undergone 12 cycles of endonuclear replication.

Drosophila nurse cells normally undergo nine or ten cycles of DNA replication and the chromatids dissociate so that each nucleus is filled with a jumbled mass of oligotene threads. In otu pseudonurse cells, the chromatids remain in register, generating banded polytene chromosomes.

The proportions of ovarioles with the different phenotypes appear to reflect the level of function of the particular allele; homozygotes are less severely affected than hemizygotes; similarly, the levels of function of certain alleles decline as the developmental temperature is raised.