Table 1.

Phenotypes with mutant Vasa homologs in Drosophila and in mice

Species	Vasa variants	Phenotype	Refs
Drosophila	VasPH165 (Vasnull)	Null allele due to entire 7343 bp deletion of coding region of vas. Vasnull ovaries have tumorous germline cysts, disrupted oocyte differentiation, fewer mature eggs	[47]
	Vas1	Hypomorphic allele generated by EMS with no mutation in coding region of Vas, but its protein is not expressed after germarium stage. Vas1 females lack polar plasm, PGC and a few posterior segments, and are inviable	[24]
	VasLYG2	P-element-induced hypomorphic vas allele due to residual 2% protein level of wildtype vas; oogenesis is less compromised with numerous laid eggs	[76]
	GFP-VasaF504E	Reduced enrichment of GFP-Vasa-F504E to the nuage of nurse cells and ubiquitous distribution in oocyte cytoplasm rescued in the vasaPD/D1	[44]
	VasW660E	VasW660E homozygous females have lower number of embryos with pole cells, disrupted embryonic patterning, mislocalization of vas in nuage and pole plasm, reduced function in piRNA biogenesis	[49]
	VasW660F	Less effect on germ cell formation and embryonic development compared to VasW660E	[49]
	Vasc.bele	Chimeric Vas with last 7 aa substituted by the C-terminal 7 aa from Vas somatic paralog Bel (DDX3). Vasc.bele exhibits granular localization in the nuage as opposed to a smooth perinuclear ring in wt, but maintains its localization to pole plasm till stage 14 with diminished eggs laid	[49]
	Vas∆3–200 or Vas∆636–646 or Vas∆655–661	Female mutants still can produce more than half number of eggs as in wildtype. Translational failure of Grk. Abnormal Vasa localization. Vas∆3–200 and Vas∆655–661 is critical for transposon control	[48]
	Walker A (Motif I): (VasG294A, VasK295N, VasT296V)	Female oogenesis was partially rescued albeit with 2 ~ threefold reduction in the egg number. Translational failure of Grk. Abnormal Vasa localization. transposon control	[48, 75]
	VasE400A	Female oogenesis was partially rescued albeit with fivefold reduction of the egg. Translational failure of Grk. Abnormal Vasa localization	[48, 75]
	VasD554A	Failure to restore female oogenesis. Translational failure of Grk. Abnormal Vasa localization	[48]
	Vas∆636–646 or Vas∆655–661	Translational failure of Grk. Abnormal Vasa localization. Vas∆655–661 is especially critical for transposon control	[48]
	VasHE(R170S), VasQ6(V465M) (aka “Vas6”), VasPW(S518F), VasAS(H520Y), VasD5(G552E), Vas3F(G587E)	Failure to localize either to the perinuclear region of the nurse cells or to the pole plasm. Disrupted formation of perinuclear granule particles	[58]
	Vas011(I256N)(aka “Vas4”), Vas4C(P268S), Vas014(I271M) (aka “Vas5”)	Vas011(I256N) localized to pole plasm at a reduced level. Vas4C(P268S) failed to localize to the pole plasm; Vas014(I271M) localized normally to both the perinuclear region and pole plasm;	[58]
Mouse	Ddx4null (Exons 9/10 KO)	Impaired meiotic initiation.Male germline ceased differentiation by the zygotene stage and underwent apoptosis. Normal female fertility	[21]
	Ddx4+/E446Q (DEAD→EQAD)	Male-specific infertility (dominant-negative effect). No derepression of TEs. Spermiogenic arrest	[51]
	Ddx4−/E446Q (DEAD→EQAD)	Phenocopied Mvh-null male testes. TEs (IAP and LINE1) activation. Incomplete meiosis. Female germline development is normal	[51]