FlyBase Allele Report: Dmel\sax[1]

The number of Kr-positive amnioserosa cells (the dorsal most embryonic fate) is reduced in the progeny of sax¹/sax² mutant mothers compared to wild-type embryos.

(Twombly et al., 2009)

Eggs laid by sax¹/+ show 100.0% wild type dorsal appendages.

(Mantrova et al., 1999)

sax¹/sax² mutant females generate embryos that show loss of the amnioserosa.

(Rusch and Levine, 1997)

sax¹/sax² individuals exhibit nearly wild type wings. When in combination with put¹³⁵ heterozygotes most individuals lack the posterior cross vein.

(Letsou et al., 1995)

Mutant embryos show ventralization of dorsal cuticle, gut defects, severe reduction in the size of imaginal discs and anterior egg shell defects.

(Brummel et al., 1994)

Embryos from sax¹/sax² females show deletions of anterodorsal head structures and an internalization of the Filzkorper and the seventh and eighth abdominal segments. This partially ventralized phenotype is characteristic of embryos from mother homozygous for weak alleles of dpp or heterozygous for null dpp allele. Heterozygous females that are also heterozygous for dpp^hr56 or dpp^hr27, show markedly reduced viability (for dpp^hr56) or lethality (for dpp^hr27). The enhancement of the mutant phenotype extends to the phenotype of the embryos produced. Transheterozygotes of tkv⁷ and sax¹ are virtually sterile.

(Nellen et al., 1994)

The presence of sax¹ in the mother causes dpp^hr27 to behave as a dominant lethal in the zygote.

(Penton et al., 1994)

Embryos from sax¹/sax² mothers have a deep dorsal cephalic furrow, and the germband does not extend to its full length dorsally.

(Xie et al., 1994)

Female sterility of homozygous mothers can be reduced by dpp duplications.

(Twombly et al., 1992)

Eggs derived from homozygous females cellularise normally but become abnormal at gastrulation. The cephalic furrow is abnormally deep at its dorsal side. The germ band does not extend its full length along the dorsal side, but buckles in under the dorsal epithelium when it is one third the distance from the posterior end. Posterior midgut invagination occurs at an abnormal dorsal position. The cuticle does not show any obvious ventralised phenotype; the denticle belts are normal in width and the dorsal hypoderm is present, although there are abnormalities in the cuticle at the anterior and posterior ends. The phenotype resembles mutations of tsg, zen and weak alleles of dpp.

(Schupbach and Wieschaus, 1989)

External Data

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Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

NOT Enhanced by

Statement

Reference

sax¹ has lethal | recessive phenotype, non-enhanceable by lilli^unspecified

(Su et al., 2001)

Suppressed by

Statement

Reference

sax¹/sax² has lethal | maternal effect | embryonic stage phenotype, suppressible | partially by Dp(2;2)DTD48/+

(Twombly et al., 2009)

sax¹/sax² has lethal | maternal effect | embryonic stage phenotype, suppressible | partially by Dp(2;2)B16/+

(Twombly et al., 2009)

sax¹/Df(2R)H23 has lethal | maternal effect | embryonic stage phenotype, suppressible by Dp(2;2)DTD48/+

(Twombly et al., 2009)

sax¹/Df(2R)H23 has lethal | maternal effect | embryonic stage phenotype, suppressible by Dp(2;2)B16/+

(Twombly et al., 2009)

dpp^hr4/dpp[+], sax¹ has lethal | dominant | maternal effect phenotype, suppressible by Dp(2;2)DTD48/+

(Twombly et al., 2009)

dpp^hr4/dpp[+], sax¹ has lethal | dominant | maternal effect phenotype, suppressible by Dp(2;2)B16/+

(Twombly et al., 2009)

Enhancer of

Statement

Reference

sax[+]/sax¹ is an enhancer of visible | dominant phenotype of Df(2L)JS17/+, dpp^d12

(Twombly et al., 2009)

Suppressor of

Statement

Reference

sax¹, Agam\gbb1^gbb.PF, sax² is a suppressor of visible phenotype of gbb⁴/gbb¹

(Fritsch et al., 2010)

sax¹, Agam\gbb2^gbb.PF, sax² is a suppressor of visible phenotype of gbb⁴/gbb¹

(Fritsch et al., 2010)

sax¹ is a suppressor of visible phenotype of upd1^GMR.PB

(Bach et al., 2003)

NOT Suppressor of

Statement

Reference

sax¹, scw^gbb.PF, sax² is a non-suppressor of visible phenotype of gbb⁴/gbb¹

(Fritsch et al., 2010)

Other

Statement

Reference

dpp^hr4/dpp[+], sax¹ has lethal | dominant | maternal effect phenotype

(Twombly et al., 2009)

dpp^e87/dpp[+], sax¹ has partially lethal - majority die | dominant phenotype

(Twombly et al., 2009)

dpp^hr56/dpp[+], sax¹ has lethal | dominant | maternal effect phenotype

(Twombly et al., 2009)

dpp[+]/dpp^hr90, sax¹ has lethal | dominant | maternal effect phenotype

(Twombly et al., 2009)

Mad¹²/Mad[+], sax¹ has lethal | dominant | maternal effect phenotype

(Twombly et al., 2009)

Df(2L)JS17/+, sax¹ has lethal | dominant | maternal effect phenotype

(Twombly et al., 2009)

sax¹, scw[+]/scw^E1 has lethal | dominant | maternal effect phenotype

(Twombly et al., 2009)

sax¹, scw^E2/scw[+] has lethal | dominant | maternal effect phenotype

(Twombly et al., 2009)

dpp^hr27/dpp[+], sax¹ has lethal | dominant | maternal effect phenotype

(Twombly et al., 2009)

dpp^hr93/dpp[+], sax¹ has lethal | dominant phenotype

(Xie et al., 1994)

dpp^hr27, sax[+]/sax¹ has lethal | dominant phenotype

(Xie et al., 1994)

dpp^hr93, sax[+]/sax¹ has lethal | dominant phenotype

(Xie et al., 1994)

dpp^hr27/dpp[+], sax¹ has lethal | dominant phenotype

(Xie et al., 1994)

Phenotype Manifest In

Suppressed by

Statement

Reference

sax¹ has phenotype, suppressible by tkv^Ubi-p63E.PB

(Brummel et al., 1994)

Enhancer of

Statement

Reference

sax[+]/sax¹ is an enhancer of unguis phenotype of Df(2L)JS17/+, dpp^d12

(Twombly et al., 2009)

sax[+]/sax¹ is an enhancer of wing vein phenotype of Df(2L)JS17/+, dpp^d12

(Twombly et al., 2009)

Suppressor of

Statement

Reference

sax¹, Agam\gbb1^gbb.PF, sax² is a suppressor of wing vein phenotype of gbb⁴/gbb¹

(Fritsch et al., 2010)

sax¹, Agam\gbb2^gbb.PF, sax² is a suppressor of wing vein phenotype of gbb⁴/gbb¹

(Fritsch et al., 2010)

sax¹ is a suppressor of eye phenotype of upd1^GMR.PB

(Bach et al., 2003)

NOT Suppressor of

Statement

Reference

sax¹, scw^gbb.PF, sax² is a non-suppressor of wing vein phenotype of gbb⁴/gbb¹

(Fritsch et al., 2010)

Other

Statement

Reference

Mef2⁴²⁴, sax¹ has egg phenotype

(Mantrova et al., 1999)

Mef2⁴²⁴, sax¹ has dorsal appendage phenotype

(Mantrova et al., 1999)

sax¹, tkv⁷ has egg phenotype

(Twombly et al., 1996)

sax¹, tkv⁷ has dorsal appendage phenotype

(Twombly et al., 1996)

dpp^d5/dpp^d6, sax¹ has prothoracic unguis phenotype

(Brummel et al., 1994)

dpp^d5/dpp^d6, sax¹ has mesothoracic unguis phenotype

(Brummel et al., 1994)

dpp^d5/dpp^d6, sax¹ has metathoracic unguis phenotype

(Brummel et al., 1994)

Additional Comments

Genetic Interactions

Statement

Reference

scw^gbb.PF cannot rescue the wing vein defects of gbb¹/gbb⁴ flies in a sax¹/sax² background.

(Fritsch et al., 2010)

The maternal effect lethal phenotype of sax¹/sax² embryos can be significantly suppressed by paternal Dp(2;2)DTD48 or Dp(2;2)B16 duplications.

The maternal effect lethal phenotype of sax¹/Df(2R)H23 embryos is suppressed by paternal Dp(2;2)DTD48 or Dp(2;2)B16 duplications.

When dpp^hr4/+ males are crossed to sax¹/+ females, all the resulting dpp^hr4/+ progeny die. Similarly, any one of the paternal dpp^e87/+, dpp^hr56/+, dpp^hr90/+ or dpp^hr27/+ genotypes in combination with a maternal sax¹/+ genotype results in increased dpp zygotic haplolethality in the progeny.

The maternal enhancement of the dpp^hr4/+ zygotic haplolethality by sax¹/+ is suppressed by either Dp(2;2)DTD48/+ or Dp(2;2)B16/.

Strong maternal effect lethality is observed when trans-heterozygous Mad¹² sax¹ females are crossed with wild-type males.

Strong maternal effect lethality is observed when trans-heterozygous Df(2L)JS17 sax¹ females are crossed with wild-type males.

sax¹/+ enhances the trans-heterozygous dpp^d12 Df(2L)JS17 phenotype characterised by missing tarsal claws and abnormal wing venation.

sax¹ heterozygous mothers generate synthetic lethality when crossed to scw^E1/+ males.

sax¹ heterozygous mothers generate synthetic lethality when crossed to scw^E2/+ males.

(Twombly et al., 2009)

Eggs laid by Mef2⁴²⁴/sax¹ females show 88.3% wild type dorsal appendages, 10.0% reduced dorsal appendages, 1.2% broad dorsal appendages and short egg length, 0.2% broad dorsal appendages and normal egg length, and 0.2% abnormal dorsal appendages with short egg length.

(Mantrova et al., 1999)

42% of the eggs produced by tkv⁷/sax¹ females have reduced dorsal appendages and 31% are short with fused appendages. The opercula are shifted towards the anterior pole, and appear to lack normal follicle cell imprint patterns.

(Twombly et al., 1996)

When the genetic background is heterozygous for sax¹, any dpp mutant phenotype is more severe than expected. Maternal effect of sax¹ can be rescued by extra dpp⁺, supplied by a duplication.

(Brummel et al., 1994)

Flies transheterozygous for dpp^hr27 or dpp^hr93 and sax¹ or sax² fail to eclose. sax mutants can be rescued by extra copies of dpp, dpp^Sal20 or dpp^P6.5.

(Xie et al., 1994)

Xenogenetic Interactions

Statement

Reference

Agam\gbb1^gbb.PF and Agam\gbb2^gbb.PF each partially rescue the wing vein defects of gbb¹/gbb⁴ animals in a sax¹/sax² background; partial rescue of the posterior crossvein is seen and in addition loss of the distal tips of vein L5 and loss of the distal quarter of vein L4 are seen.

(Fritsch et al., 2010)

Complementation and Rescue Data

Comments

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

98354

sax¹ cn¹ bw¹ speck¹/CyO

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (5)

Reported As

Symbol Synonym

sax¹

(Quijano et al., 2011, Ellis et al., 2010, Fritsch et al., 2010, Twombly et al., 2009)

sax^W0

(Schupbach and Wieschaus, 1989)

sax^WO18

(Yip et al., 1997)

sax^WO

sax^Wo

(Johannes and Preiss, 2002)

Name Synonyms

Secondary FlyBase IDs

References (23)

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