FlyBase Allele Report: Dmel\Sas-4[s2214]

(Gallaud et al., 2014, Gopalakrishnan et al., 2011, Nguyen et al., 2011, Basto et al., 2008, Rodrigues-Martins et al., 2008, Basto et al., 2006, Toub, 2003.10.22, Spradling et al., 1999, BDGP Project Members, 1994-1999)

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

Expression Data

Reporter Expression

Additional Information

Statement

Reference

Marker for

Reflects expression of

Reporter construct used in assay

Human Disease Associations

Disease Ontology (DO) Annotations

Models Based on Experimental Evidence ( 1 )

Disease

Evidence

References

model of primary autosomal recessive microcephaly 6

CEA

(Zheng et al., 2014)

model of microcephaly

CEA with mad2^G6595

(Poulton et al., 2017)

CEA

(Basto et al., 2006)

Modifiers Based on Experimental Evidence ( 1 )

Disease

Interaction

References

exacerbates microcephaly

modeled by Mad1¹

(Poulton et al., 2017)

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

abnormal cell cycle | somatic clone

(Januschke and Gonzalez, 2010)

abnormal cell polarity | somatic clone

(Januschke and Gonzalez, 2010)

abnormal cytokinesis

(Gallaud et al., 2014)

abnormal developmental rate

(Basto et al., 2008)

abnormal mating

(Basto et al., 2006)

abnormal meiotic cell cycle

(Rodrigues-Martins et al., 2008)

abnormal mitotic cell cycle

(Gallaud et al., 2014, Basto et al., 2006)

abnormal mitotic cell cycle | third instar larval stage

(Poulton et al., 2017, Caous et al., 2015)

increased cell number | third instar larval stage

(Poulton et al., 2017)

increased occurrence of cell division | third instar larval stage

(Caous et al., 2015)

lethal

(Basto et al., 2006)

lethal | recessive

(Spradling et al., 1999, BDGP Project Members, 1994-1999)

male sterile

(Basto et al., 2006)

neoplasia | third instar larval stage

(Caous et al., 2015)

short lived

(Basto et al., 2006)

some die during immature adult stage | recessive

(Basto et al., 2006)

uncoordinated

(Basto et al., 2006)

uncoordinated (with Sas-4^Δ90)

(Gopalakrishnan et al., 2011)

uncoordinated (with Sas-4^Δ150)

(Gopalakrishnan et al., 2011)

uncoordinated (with Sas-4^ΔPN2-3)

(Gopalakrishnan et al., 2011)

uncoordinated | recessive

(Gopalakrishnan et al., 2011)

Phenotype Manifest In

aster, with Sas-4^ΔT.GFP

(Gopalakrishnan et al., 2012)

central protocerebral neuroblast | third instar larval stage

(Poulton et al., 2017)

centriole

(Blachon et al., 2009, Rodrigues-Martins et al., 2008, Basto et al., 2006)

centriole | progressive

(Galletta et al., 2016)

centrosome

(Gopalakrishnan et al., 2011, Basto et al., 2006)

ciliary rootlet

(Chen et al., 2015)

cilium

(Basto et al., 2006)

embryonic/larval brain

(Gallaud et al., 2014)

larval neuroblast | increased number | third instar larval stage

(Caous et al., 2015)

male germline stem cell | progressive

(Galletta et al., 2016)

mitotic spindle | third instar larval stage

(Caous et al., 2015)

motile cilium

(Basto et al., 2006)

neuroblast

(Gallaud et al., 2014, Basto et al., 2006)

primary spermatocyte

(Rodrigues-Martins et al., 2008)

sensory neuron | embryonic stage 16

(Nguyen et al., 2011)

spermatid

(Blachon et al., 2009)

spermatid axoneme, with Sas-4^ΔT.GFP

(Gopalakrishnan et al., 2012)

spermatozoon

(Gopalakrishnan et al., 2012)

spindle

(Gallaud et al., 2014, Rodrigues-Martins et al., 2008)

Detailed Description

Statement

Reference

Sas-4^s2214 homozygous third instar larval brains do not display obvious defects in volume, overall tissue organization (including overall layer size and organization, size and organization of medullar axons, and number of neuroepithelial cells), proportions of apoptotic cells (assessed by Hid-GFP, cleaved Casp-3 and cleaved Dcp-1), mitotic cells and DNA-damaged cells, but their central brain neuroblasts display small but significant increases in number and in the frequency of ploidy defects and a delayed entry into anaphase, as compared to controls.

(Poulton et al., 2017)

As development proceeds (larvae 72 and 96 after egg laying, pharate adults) the centrioles are being lost from male germline stem cells in Sas-4^s2214 homozygotes but the centriole length is normal compared to controls.

(Galletta et al., 2016)

Sas-4^s2214 homozygous larvae display highly increased number of brain neuroblasts and slightly increased mitotic index but the brain size remains normal, the neuroblast often display mitotic spindle alignment defects but the rate of aneu- or polyploidy in the brain cells is only mildly increased compared to controls. The mutant brain tissue shows the ability to induce tumor formation in an tissue allograft assay, albeit with low efficiency.

(Caous et al., 2015)

Ciliary rootlets are absent from most olfactory neurons and from most chordotonal organs of the Johnston's organ in mutant adults.

(Chen et al., 2015)

In Sas-4^s2214 single mutants, the spindle forms without centrosomes and mitosis lasts for approximately 9 minutes. After cold treatment, which depolymerises microtubules, Sas-4^s2214 single mutants exhibit wild-type microtubule regrowth. Bipolar spindle assembly occurs within 3 minutes in flies lacking Sas-4^s2214, as in wild-type.

(Gallaud et al., 2014)

The sperm axonemes of Sas-4^s2214 males rescued with Sas-4^{ΔT.T:Avic\GFP} are abnormal, but the number of centrosomes is normal. Interphase spermatocyte centrosomes show premature microtubule nucleation and meiotic centrosomes have massive microtubule asters, which can fill a significant fraction of the cell. Over 95% of round spermatids show normal morphology, suggesting that meiotic cell division can conclude normally.

(Gopalakrishnan et al., 2012)

Sas-4^s2214 mutant stage 16 embryos still exhibit centrioles in many sensory neurons. While most neurons exhibit sensory cilia with normal morphology, about 20% exhibit either no cilia or truncated cilia.

No significant difference in the direction of centriole comet movement is found in Sas-4^s2214 mutant larval sensory neurons. The morphology of Sas-4^s2214 mutant ddaE dendrites is as in controls.

(Nguyen et al., 2011)

Approximately 25% of Sas-4^s2214 mutant neuroblasts fail asymmetric cell division. The orientation of cortical polarity and cell division changes by 90% from one mitosis to the next in Sas-4^s2214 MARCM clones. Changes occur consistently in one direction.

(Januschke and Gonzalez, 2010)

Mutant centrioles are abnormally short, though the proximal centriole-like structure is present in spermatids.

(Blachon et al., 2009)

Homozygous Sas-4^s2214 mutant flies show a slight delay in development.

(Basto et al., 2008)

Virtually all Sas-4^s2214 mutant primary spermatocytes lack centrioles. All of the acentriolar spindles analysed are abnormal and these abnormal spindles result in dramatic chromosome segregation defects. Spermatids from Sas-4^s2214 mutants frequently have multiple nuclei of differing sizes indicative of unequal partitioning of chromosomes in meiosis.

(Rodrigues-Martins et al., 2008)

Sas-4^s2214 mutant third-instar larval brains lack both centrioles and centrosomes. Analysis of the development of Sas-4^s2214 animals laid by Sas-4^s2214/+ mothers shows that centrioles are lost during development. In stage 15-16 embryos, ~50-80% of cells have no detectable centrioles. By the first larval instar, centrioles are detectable in only ~10% of cells.

Although Sas-4^s2214 larvae and pupae lack centrioles, Sas-4^s2214 morphologically-normal flies eclose at near-normal rates. However, these flies are severely uncoordinated, leading to an ability to hold their wings or legs in a normal position and the propensity to get stuck in food and die soon after eclosion. When Sas-4^s2214 flies eclose away from food, they survive for several days before dying of dehydration. The lack of centrioles in these flies means that they also lack cilia and the lack of these cilia in the mechanosensory neurons may account for their uncoordination. Sas-4^s2214 sperm also lack centrioles and flagella.

Sas-4^s2214 cells in third-instar larval brains are unable to form centrosomes during mitosis and show few organized microtubule arrays at early stages of mitosis. As mitosis proceeds, the microtubules polymerize around the mitotic chromatin and become organized into bipolar spindles. These acentrosomal spindles appear to segregate chromosomes normally as there is only a small increase in the proportion of Sas-4^s2214 aneuploid cells. The mitotic index is slightly increased in Sas-4^s2214 brains, suggesting that the length of mitosis is extended by 30-40%.

Asymmetric cell division is disrupted in ~30% of Sas-4^s2214 larval neuroblasts. The acentrosomal spindles in dividing Sas-4^s2214 neuroblasts are often mispositioned within the cell, and as a result, many cells go through phases of irregular shape changes. Around 15% of neuroblasts divide asymmetrically and around another 15% fail to complete cell division. Of the majority of Sas-4^s2214 neuroblasts that do divide asymmetrically, the size difference between some of the daughter cells is less obvious than between wild-type daughter cells. However, the distribution of neurons, neuroblasts and axons are grossly normal in Sas-4^s2214 tissues.

(Basto et al., 2006)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

Sas-4^s2214 has abnormal mitotic cell cycle | third instar larval stage phenotype, enhanceable by mad2^G6595/mad2^G6595

(Poulton et al., 2017, Caous et al., 2015)

Sas-4^s2214 has abnormal mitotic cell cycle | third instar larval stage phenotype, enhanceable by BubR1^k06109/BubR1^KEN.mRFP1

(Caous et al., 2015)

Sas-4^s2214 has abnormal cytokinesis phenotype, enhanceable by ens^HP36480

(Gallaud et al., 2014)

Sas-4^s2214 has abnormal mitotic cell cycle phenotype, enhanceable by ens^HP36480

(Gallaud et al., 2014)

NOT Enhanced by

Statement

Reference

Sas-4^s2214 has abnormal developmental rate phenotype, non-enhanceable by SAK^Ubi.GFP

(Basto et al., 2008)

Suppressed by

Statement

Reference

Sas-4^s2214, mad2^G6595 has abnormal neuroanatomy | third instar larval stage phenotype, suppressible | partially by Scer\GAL4^insc-Mz1407/BacA\p35^UAS.cHa

(Poulton et al., 2017)

Sas-4^s2214, mad2^G6595 has abnormal size | third instar larval stage phenotype, suppressible | partially by Scer\GAL4^insc-Mz1407/BacA\p35^UAS.cHa

(Poulton et al., 2017)

Sas-4^s2214 has neoplasia | third instar larval stage phenotype, suppressible by mad2^G6595/mad2^G6595

(Caous et al., 2015)

Enhancer of

Statement

Reference

Sas-4^s2214/Sas-4^s2214 is an enhancer of abnormal neuroanatomy | third instar larval stage phenotype of Df(2R)w45-30n/Mad1¹

(Poulton et al., 2017)

Sas-4^s2214/Sas-4^s2214 is an enhancer of abnormal size | third instar larval stage phenotype of Df(2R)w45-30n/Mad1¹

(Poulton et al., 2017)

Sas-4^s2214/Sas-4^s2214 is an enhancer of abnormal mitotic cell cycle | third instar larval stage phenotype of BubR1^KEN.mRFP1, BubR1^k06109

(Caous et al., 2015)

Sas-4^s2214 is an enhancer of abnormal mitotic cell cycle phenotype of ens^HP36480

(Gallaud et al., 2014)

Sas-4^s2214 is an enhancer of abnormal cytokinesis phenotype of ens^HP36480

(Gallaud et al., 2014)

Suppressor of

Statement

Reference

Sas-4^s2214 is a suppressor of abnormal developmental rate phenotype of SAK^Ubi.GFP

(Basto et al., 2008)

Other

Statement

Reference

Sas-4^s2214, mad2^G6595 has decreased cell number | third instar larval stage phenotype

(Poulton et al., 2017)

Sas-4^s2214, mad2^G6595 has lethal - all die before end of prepupal stage phenotype

(Poulton et al., 2017)

Sas-4^s2214, mad2^G6595 has increased cell size | third instar larval stage phenotype

(Poulton et al., 2017)

Sas-4^s2214, mad2^G6595 has abnormal developmental rate phenotype

(Poulton et al., 2017)

Sas-4^s2214, mad2^G6595 has abnormal neuroanatomy | third instar larval stage phenotype

(Poulton et al., 2017)

Sas-4^s2214, mad2^G6595 has abnormal size | third instar larval stage phenotype

(Poulton et al., 2017)

Sas-4^s2214, mad2^G6595 has increased cell death | recessive | third instar larval stage phenotype

(Poulton et al., 2017)

Sas-4^s2214, mad2^G6595 has increased cell number | third instar larval stage phenotype

(Poulton et al., 2017)

Sas-4^s2214, aurA⁸⁸³⁹, mad2^G6595 has abnormal mitotic cell cycle | third instar larval stage phenotype

(Caous et al., 2015)

Grip71¹²⁰, Sas-4^s2214 has lethal | pupal stage phenotype

(Reschen et al., 2012)

Grip75¹⁷⁵, Sas-4^s2214 has lethal | pupal stage phenotype

(Reschen et al., 2012)

Sas-4^s2214, wac^unspecified has lethal | pupal stage phenotype

(Reschen et al., 2012)

Phenotype Manifest In

Enhanced by

Statement

Reference

Sas-4^s2214 has mitotic spindle | third instar larval stage phenotype, enhanceable by mad2^G6595/mad2^G6595

(Caous et al., 2015)

Sas-4^s2214 has embryonic/larval brain phenotype, enhanceable by ens^HP36480

(Gallaud et al., 2014)

Sas-4^s2214 has spindle phenotype, enhanceable by ens^HP36480

(Gallaud et al., 2014)

Sas-4^s2214 has neuroblast phenotype, enhanceable by ens^HP36480

(Gallaud et al., 2014)

Suppressed by

Statement

Reference

Sas-4^s2214 has larval neuroblast | increased number | third instar larval stage phenotype, suppressible by mad2^G6595/mad2^G6595

(Caous et al., 2015)

Sas-4^s2214 has larval neuroblast | increased number | third instar larval stage phenotype, suppressible by BubR1^k06109/BubR1^KEN.mRFP1

(Caous et al., 2015)

Enhancer of

Statement

Reference

Sas-4[+]/Sas-4^s2214 is an enhancer of female germline cyst phenotype of vih^ΔN-9

(Braun et al., 2021)

Sas-4[+]/Sas-4^s2214 is an enhancer of plasma membrane | oogenesis phenotype of vih^ΔN-9

(Braun et al., 2021)

Sas-4^s2214 is an enhancer of embryonic/larval brain phenotype of ens^HP36480

(Gallaud et al., 2014)

Sas-4^s2214 is an enhancer of spindle phenotype of ens^HP36480

(Gallaud et al., 2014)

Sas-4^s2214 is an enhancer of neuroblast phenotype of ens^HP36480

(Gallaud et al., 2014)

NOT Enhancer of

Statement

Reference

Sas-4^s2214/Sas-4^s2214 is a non-enhancer of larval neuroblast | third instar larval stage | increased number phenotype of aurA⁸⁸³⁹, mad2^G6595

(Caous et al., 2015)

Suppressor of

Statement

Reference

Sas-4^s2214 is a suppressor of centrosome | increased number phenotype of SAK^Ubi.GFP

(Sabino et al., 2011)

Sas-4^s2214 is a suppressor of neuroblast phenotype of SAK^Ubi.GFP

(Sabino et al., 2011)

Other

Statement

Reference

Sas-4^s2214, mad2^G6595 has axon | third instar larval stage phenotype

(Poulton et al., 2017)

Sas-4^s2214, mad2^G6595 has lamina | third instar larval stage phenotype

(Poulton et al., 2017)

Sas-4^s2214, mad2^G6595 has medulla | third instar larval stage phenotype

(Poulton et al., 2017)

Sas-4^s2214, mad2^G6595 has embryonic/larval optic lobe | third instar larval stage phenotype

(Poulton et al., 2017)

Sas-4^s2214, mad2^G6595 has larval optic neuroblast | third instar larval stage phenotype

(Poulton et al., 2017)

Sas-4^s2214, mad2^G6595 has optic lobe neuroepithelial cell | third instar larval stage phenotype

(Poulton et al., 2017)

Sas-4^s2214, mad2^G6595 has adult optic lobe neuron | third instar larval stage phenotype

(Poulton et al., 2017)

Sas-4^s2214, mad2^G6595 has central protocerebral neuroblast | third instar larval stage phenotype

(Poulton et al., 2017)

Sas-4^s2214, mad2^G6595 has outer optic anlage neuroblast | third instar larval stage phenotype

(Poulton et al., 2017)

Df(2R)w45-30n/Mad1¹, Sas-4^s2214 has medulla | third instar larval stage phenotype

(Poulton et al., 2017)

Df(2R)w45-30n/Mad1¹, Sas-4^s2214 has central protocerebral neuroblast | third instar larval stage phenotype

(Poulton et al., 2017)

Sas-4^s2214, mad2^G6595 has embryonic/larval brain | third instar larval stage phenotype

(Poulton et al., 2017)

SAK^Ubi.GFP, Sas-4^s2214 has centriole phenotype

(Basto et al., 2008)

Additional Comments

Genetic Interactions

Statement

Reference

Sas-4^s2214, mad2^G6595 double homozygotes exhibit a developmental delay, until arresting and dying at the larval\pupal transition, as compared to controls. Their third instar larval, but not second instar larval or embryonic, brains display a severe decrease in overall volume, a severe increase in the proportion of apoptotic cells (assessed by Hid-GFP, cleaved Casp-3 and Dcp-1), a severe increase in the overall mitotic index (including of the central brain neuroblast population), and a significant increase in the proportion of DNA damaged cells, as compared to controls. Third instar larval brains also display severe tissue organization defects, which mostly affect the optic lobes, as compared to controls: loss or strong reduction of the medulla layer, which exhibits very few neuroblasts and decreased numbers of disorganized neuroepithelial cells; apparent loss of the lamina layer; decreased size of the medullar neuropil, associated with decreased size and disorganization of the axons from medullar neurons; decreased size and complexity of the outer optic anlagen (but not at the second instar larval stage); decreases in number and in organization of central brain neuroblasts, which are able to divide symmetrically, but occasionally exhibit an increased cell size and differentiation defects (i.e. expressing both Dpn and Pros proteins); but not any obvious defects in the mushroom body. The frequency of ploidy defects observed in Sas-4^s2214-homozygous third instar larval central brain neuroblasts is strongly enhanced by mad2^G6595 homozygosity.

Homozygosity for Sas-4^s2214 strongly enhances the decreased brain volume phenotype observed in Mad1¹/Df(2R)w45-30n transheterozygous third instar larvae; these double mutant brains exhibit loss or strong reduction of the medulla, and high disorganization of the central brain neuroblasts, as compared to single mutants and wild-type controls.

(Poulton et al., 2017)

The increased brain neuroblast (NB) number observed in Sas-4^s2214 mutant third instar larvae is fully suppressed by combination with mad2^G6595 (the NB number in the double mutants is even lower than in wild-type controls and the brains are also smaller), while the NB mitotic spindle defects are enhanced and numerous aneuploid or polyploid cells are frequently observed. The double mutant brain tissue also cannot (unlike that from Sas-4^s2214 single mutants) induce tumor formation in an allograft assay. Similarly, the number of NBs in Sas-4^s2214;BubR1^{KEN.T:Disc\RFP-mRFP},BubR1^k06109 double mutant larval brains is also even lower than in wild-type while the rate of ploidy defects is strongly increased compared to either of the single gene mutants.

aurA⁸⁸³⁹;Sas-4^s2214;mad2^G6595 triple mutants show high rate of ploidy defects in third instar larval brains, the number of neuroblasts or the mitotic cells is highly increased relative to wild-type but significantly different from aurA⁸⁸³⁹;Sas-4^s2214 double mutants.

(Caous et al., 2015)

In ens^HP36480,Sas-4^s2214 double mutants, mitosis lasts for approximately 10 minutes (longer than in the Sas-4^s2214 single mutant) and the distribution of microtubules is more strongly affected than in the single mutant. The spindles are much shorter than in either single mutant. After cold treatment, which depolymerises microtubules, ens^HP36480,Sas-4^s2214 double mutants exhibit compromised microtubule regrowth, as in ens^HP36480 single mutants. Bipolar spindle assembly is severely compromised in these double mutants.

(Gallaud et al., 2014)

The generation of supernumerary centrosomes in SAK^{Ubi.T:Avic\GFP} mutant neuroblasts is suppressed by a Sas-4^s2214 background.

(Sabino et al., 2011)

Homozygous Sas-4^s2214 partially suppresses the developmental delay seen in flies expressing SAK^{Ubi.T:Avic\GFP}, producing a slight delay as is seen in Sas-4^s2214 mutants alone. Eclosion occurs at a similar rate to wild type. As in Sas-4^s2214 mutants, the flies contain no detectable centrioles.

(Basto et al., 2008)

Xenogenetic Interactions

Statement

Reference

The decreased brain volume of Sas-4^s2214, mad2^G6595 double homozygous third instar larvae is partially suppressed by the expression of BacA\p35^Scer\UAS.cHa under the control of Scer\GAL4^insc-Mz1407.

(Poulton et al., 2017)

Complementation and Rescue Data

Rescued by

Sas-4^s2214 is rescued by Sas-4^+mGa

(Gopalakrishnan et al., 2011)

Partially rescued by

Sas-4^s2214 is partially rescued by Sas-4^ΔT.GFP

(Gopalakrishnan et al., 2012)

Sas-4^s2214 is partially rescued by Sas-4^Δ90

(Gopalakrishnan et al., 2011)

Sas-4^s2214 is partially rescued by Sas-4^ΔPN2-3

(Gopalakrishnan et al., 2011)

Not rescued by

Sas-4^s2214 is not rescued by Sas-4^Δ150

(Gopalakrishnan et al., 2011)

Comments

Sas-4^{ΔT.T:Avic\GFP} fails to fully rescue the Sas-4^s2214 phenotype of uncoordination: the flies stand but can barely walk.

(Gopalakrishnan et al., 2012)

Sas-4^ΔPN2-3 partially rescues the Sas-4^s2214 uncoordinated phenotype. Flies expressing Sas-4^ΔPN2-3 in a Sas-4^s2214 mutant background are unable to stand.

Sas-4^Δ90 partially rescues the Sas-4^s2214 uncoordinated phenotype. Flies expressing Sas-4^Δ90 in a Sas-4^s2214 mutant background are able to walk almost normally.

Sas-4^Δ150 fails to rescue the Sas-4^s2214 uncoordinated phenotype.

Sas-4^+mGa rescues the Sas-4^s2214 uncoordinated phenotype.

Unlike Sas-4^s2214 mutants, flies expressing Sas-4^Δ90 have normal number of centrosomes.

Unlike Sas-4^s2214 mutants, flies expressing Sas-4^ΔPN2-3 have normal number of centrosomes.

(Gopalakrishnan et al., 2011)

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

12119

w¹¹¹⁸; P{lacW}Sas-4^s2214/TM3, Sb¹

Notes on Origin

Discoverer

M. Scott.

Comments

Complements: Alh^j13A6. Complements: Alh^j5B1. Complements: Alh^j8C8.

(BDGP Project Members, 1994-1999)

Precise excision of the P{lacW} element reverts the phenotypes observed in Sas-4^s2214 mutants.

(Basto et al., 2006)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (20)

Reported As

Symbol Synonym

DSas-4^S2214

(Januschke and Gonzalez, 2010, Basto et al., 2006)

DSas-4^s2214

(Franz et al., 2013)

Dsas4^S2214

(Reschen et al., 2012)

Dsas4^s2214

(Song et al., 2023)

Sas-4²²¹⁴

(Ricolo et al., 2016)

Sas-4^S2214

(Chen et al., 2015, Taniguchi et al., 2014)

Sas-4^s2214

(Gambarotto et al., 2019, Ramani et al., 2018, Baumbach et al., 2015, Nguyen et al., 2011)

Sas-4s2214

(Gopalakrishnan et al., 2011)

Sas4^S2214

(Novak et al., 2016)

dsas-4^l(3)s2214

(Wang et al., 2011)

l(3)s2214

(Spradling et al., 1999)

l(3)s2214^s2214

(Gresens and Cook, 2006.12.5)

sas-4²²¹⁴

(Conduit et al., 2015)

sas-4^I(3)2214

(Cunningham et al., 2022)

sas-4^S2214

(Jauffred et al., 2013, Gopalakrishnan et al., 2012, Blachon et al., 2009)

sas-4^s2214

(Thomas et al., 2021, Zheng et al., 2020, Jo et al., 2019, Poulton et al., 2017, Caous et al., 2015, Zheng et al., 2014, Gopalakrishnan et al., 2011)

sas4^M

(Roubinet et al., 2017)

sas4^S2214

(Galletta et al., 2016, Novak et al., 2014)

sas4^mut

(Goupil et al., 2022)

sas4^s2214

(Braun et al., 2021, Lapart et al., 2019, Becker et al., 2016)

Name Synonyms

Secondary FlyBase IDs

FBal0011146
FBal0195439

References (47)

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