FlyBase Allele Report: Dmel\ct[C145]

ct^C145 mutant clones at the ureter region contain both ectopic Pros-positive enteroendocrine-like cells and ectopic Pdm1-positive enterocyte-like cells, as compared to controls.

(Xu et al., 2018)

An increased frequency of ct^C145 mutant wing disc clones (induced during either the second or third instar larval stages) respect the interface between boundary and non-boundary cell compared to wild type.

(Becam et al., 2011)

Cell polarity is not affected in ct^C145 mutant embryos.

(Campbell et al., 2009)

Homozygous clones in the antenna can result in defects in the joint cuticle at the a2/a3 joint. In antenna with large homozygous clones, the internal cuticular structures are completely absent. When the aristae of these mutants are stimulated with a paintbrush or forceps, a3 does not rotate within a2.

Animals containing homozygous clones in the antenna show a lower amplitude response in the antennal nerve (similar to background noise) than wild-type flies in response to a pulse-song, indicating that they are deaf.

Scolopidia form in homozygous clones in the pupal antenna, but they are abnormal in their organisation and reduced in number compared to wild type. In adults carrying large homozygous clones in the antenna, neurons and scolopale cells are rarely seen within a2. Vacuolated degenerated cells are present in a3.

Adults carrying large homozygous clones in the antenna show an incompletely penetrant phenotype involving transformation of the arista to tarsal identity; in 8% of cases the arista is partially transformed to distal leg, while in 11% of cases the transformation is more complete and includes tarsal claws.

(Ebacher et al., 2007)

Homozygous ct^C145 mutant clones display a marked reduction of dendrite outgrowth and branching. Dendritic termini are concentrated nearer to the cell body than in wild-type.

(Jinushi-Nakao et al., 2007)

Lateral antennal lobe projection neurons (lPN) in ct^C145 homozygous somatic clones fail to target DMA, DM2 and VA5 antennal glomeruli. Mis-targeted lPN dendrites are biased towards more lateral glomeruli than in wild-type. The number of ventral antennal projection neurons (vPN) is severely reduced in these clones and those remaining mis-target their dendrites to the subesophageal ganglion. ct^Scer\UAS.cPa; Scer\GAL4^GH146 completely rescues the targeting of DMA, DM2 and VA5 by lPN in these animals but fails to rescue the decrease in vPN cell number and only partially rescues vPN targeting VA1lm but not to DA1.

(Komiyama and Luo, 2007)

When single cell clones are made in multidendritic neurons show a dramatic defect in higher order branching and elongation, resulting in a highly reduced dendritic field. ddaA neurons show slightly less extreme phenotypes than ddaF. ddaA do not have 'spikes'. ldaB occasionally show a severe growth phenotype, but more often show an absence or severe reduction in total dendritic length and number of branch points. A lack of spikes is also the dominant phenotype of v'pda. ddaC neurons show decreased branching and elongation, though the severity of these defects are highly variable. The most severely affected neurons extend a 'skeleton' of the normal arbor with a complete loss of higher order branches and a reduced overall dendrite length. ddaB show a severe and completely penetrant decrease in dendrite growth. ldaA and the ventral neurons show variable reductions in branching. However ddaD and ddaE show normal dendrite morphologies.

(Grueber et al., 2003)

In egg chambers containing ct^C145 homozygous follicle cell clones, nurse cells with two nuclei and a spot of filamentous actin containing material can be found. These binucleate cells can be found at any position and among any of the nurse cells in the egg chamber. Most of the affected egg chambers contain a single binucleate cell, although occasionally more than one binucleate cell is present. Occasionally more than two nuclei are seen in a single cell. A clone in which approximately 25-30% of follicle cells are homozygous for ct^C145 is sufficient to produce an egg chamber with binucleate cells. Binucleate cells are not seen prior to stage 5 and are observable in stage 10 egg chambers as soon as 4 days after clonal induction. In egg chambers containing binucleate cells, ring canals at various stages of degeneration are seen, ranging from free-floating, detached, round ring canals to dense actin-containing spots. The total number of normal ring canals and degenerating ring canal remnants in these egg chambers is 15, suggesting that there is no net change in the number of cystoblast cytokineses.

(Jackson and Berg, 1999)

At 18^oC ct^L188/ct^C145 is essentially lethal, whereas at 24^oC ~50% flies eclose and appear morphologically normal.

(Johnston et al., 1998)

Egg chambers containing somatic clones of homozygous ct^C145 cells exhibit a number of phenotypes. The homozygous clones in the follicle epithelium contain 2 to 5 times fewer cells than their corresponding wild-type twin clones. The cells in the clone and their nuclei are larger than surrounding heterozygous or wild-type cells. 44% of ovarioles studied 7 days after induction of the somatic clones contain germaria that are greatly reduced in size or absent. 4 days after induction of the somatic clones, more than 50% of stage 6 and older egg chambers contain nurse cells with multiple nuclei. These egg chambers contain at least 30% homozygous ct^C145 follicle cells. 7-14 days after induction of the somatic clones, egg chambers containing abnormal numbers of germline derived nuclei are seen. This phenotype is seen in less than 1% of cases.

(Jackson and Blochlinger, 1997)

Convergence-extension movements in the Malpighian tubules are prevented.

(Tepass et al., 1996)

Lethal in combination with ct^L188.

(Ostrow and Blochlinger, 1995)

Homozygous embryos do not form es organs (FBrf0045757). In the presence of P{hsp(sE)-poxn} embryos still do not form any detectable external sensory organs.

(Vervoort et al., 1995)

Embryonic muscle phenotype wild type.

(Drysdale et al., 1993)

Lethality occurs during embryonic and early larval stages. Transformation of es organs to ch-like, scolopales are visible and external structures are missing. ch neurons are the same as in wild type.

(Merritt et al., 1993)

Expression of ct^LS enhancer trap lines in a ct^C145 mutant background demonstrates that some of the markers for Malpighian tubule cells alter their expression. Kr and cad expression in the tubules remains unchanged.

(Liu and Jack, 1992)

es organs are transformed to as ch identity, scolopales are present.

(Blochlinger et al., 1991)

Homozygous embryos lack Malpighian tubules and the gut wall is 3--4 fold thicker than wild type at the junction of the posterior and anterior midgut.

(Liu et al., 1991)

Sense organ es to ch transformation.

(Blochlinger et al., 1990)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

ct^C145 has visible | somatic clone phenotype, enhanceable by ss^a

(Ebacher et al., 2007)

Suppressed by

Statement

Reference

ct^C145 has abnormal neuroanatomy | somatic clone phenotype, suppressible by Lim1^UAS.cTa/Scer\GAL4^GH146

(Komiyama and Luo, 2007)

Enhancer of

Statement

Reference

ct[+]/ct^C145 is an enhancer of lethal | recessive | partially phenotype of mir-bft⁶

(Hardiman et al., 2002)

Other

Statement

Reference

ct[+]/ct^C145, mir-bft⁶ has lethal | recessive phenotype

(Hardiman et al., 2002)

ct^C145, mir-bft⁶ has lethal | recessive phenotype

(Hardiman et al., 2002)

Df(1)sd72b, ct^C145 has visible | dominant phenotype

(Jackson and Berg, 1999)

Df(1)A209, ct^C145 has visible | dominant phenotype

(Jackson and Berg, 1999)

Df(1)JA26, ct^C145 has lethal phenotype

(Jackson and Berg, 1999)

Df(3R)P14, ct^C145 has lethal phenotype

(Jackson and Berg, 1999)

Df(3R)Tl-P, ct^C145 has partially lethal phenotype

(Jackson and Berg, 1999)

Antp², ct^C145 has visible phenotype

(Johnston et al., 1998)

Antp^CB, ct^C145 has visible phenotype

(Johnston et al., 1998)

Antp^R, ct^C145 has visible phenotype

(Johnston et al., 1998)

Antp^Wu, ct^C145 has visible phenotype

(Johnston et al., 1998)

Antp²⁵, ct^C145 has visible phenotype

(Johnston et al., 1998)

Antp¹¹, ct^C145 has visible phenotype

(Johnston et al., 1998)

Antp¹⁶, ct^C145 has visible phenotype

(Johnston et al., 1998)

Antp²², ct^C145 has visible phenotype

(Johnston et al., 1998)

Antp^73b, ct^C145 has visible phenotype

(Johnston et al., 1998)

Antp¹¹, ct^L188/ct^C145 has visible phenotype

(Johnston et al., 1998)

Phenotype Manifest In

Enhanced by

Statement

Reference

ct^C145 has arista | somatic clone phenotype, enhanceable by ss^a

(Ebacher et al., 2007)

ct^C145 has leg | ectopic | somatic clone phenotype, enhanceable by ss^a

(Ebacher et al., 2007)

ct^C145 has phenotype, enhanceable by capu[+]/capu^HK3

(Jackson and Berg, 1999)

ct^C145 has phenotype, enhanceable by otu¹¹

(Jackson and Berg, 1999)

ct^C145 has egg chamber phenotype, enhanceable by Df(1)JC70/+

(Jackson and Berg, 1999)

ct^C145 has egg chamber phenotype, enhanceable by Df(1)RA2/+

(Jackson and Berg, 1999)

ct^C145 has egg chamber phenotype, enhanceable by Df(1)KA14/+

(Jackson and Berg, 1999)

ct^C145 has egg chamber phenotype, enhanceable by Df(1)N105/+

(Jackson and Berg, 1999)

ct^C145 has egg chamber phenotype, enhanceable by Df(1)JA26/+

(Jackson and Berg, 1999)

ct^C145 has egg chamber phenotype, enhanceable by Df(2L)30A-C/+

(Jackson and Berg, 1999)

ct^C145 has egg chamber phenotype, enhanceable by +/Df(2R)44CE

(Jackson and Berg, 1999)

ct^C145 has egg chamber phenotype, enhanceable by Df(2R)eve/+

(Jackson and Berg, 1999)

ct^C145 has egg chamber phenotype, enhanceable by Df(2R)or-BR6/+

(Jackson and Berg, 1999)

ct^C145 has egg chamber phenotype, enhanceable by Df(2R)M60E/+

(Jackson and Berg, 1999)

ct^C145 has egg chamber phenotype, enhanceable by Df(3L)GN50/+

(Jackson and Berg, 1999)

ct^C145 has egg chamber phenotype, enhanceable by Df(3L)GN24/+

(Jackson and Berg, 1999)

ct^C145 has egg chamber phenotype, enhanceable by Df(3L)66C-G28/+

(Jackson and Berg, 1999)

ct^C145 has egg chamber phenotype, enhanceable by Df(3L)AC1/+

(Jackson and Berg, 1999)

ct^C145 has egg chamber phenotype, enhanceable by Df(3L)W4/+

(Jackson and Berg, 1999)

ct^C145 has egg chamber phenotype, enhanceable by Df(3R)Antp17/+

(Jackson and Berg, 1999)

ct^C145 has egg chamber phenotype, enhanceable by Df(3R)P14/+

(Jackson and Berg, 1999)

ct^C145 has egg chamber phenotype, enhanceable by Df(3R)Tl-P/+

(Jackson and Berg, 1999)

ct^C145 has egg chamber phenotype, enhanceable by Df(1)otu-PΔ1/+

(Jackson and Berg, 1999)

ct^C145 has egg chamber phenotype, enhanceable by otu[+]/otu¹¹

(Jackson and Berg, 1999)

NOT Enhanced by

Statement

Reference

ct^C145 has epidermal cell phenotype, non-enhanceable by crb^8F105

(Campbell et al., 2009)

ct^C145 has phenotype, non-enhanceable by chic[+]/chic⁰⁷⁸⁸⁶

(Jackson and Berg, 1999)

ct^C145 has phenotype, non-enhanceable by Src64B^Δ17/Src64B[+]

(Jackson and Berg, 1999)

ct^C145 has phenotype, non-enhanceable by qua[+]/qua⁹

(Jackson and Berg, 1999)

ct^C145 has phenotype, non-enhanceable by Egfr[+]/Egfr^f24

(Jackson and Berg, 1999)

ct^C145 has phenotype, non-enhanceable by Btk29A[+]/Btk^k00206

(Jackson and Berg, 1999)

ct^C145 has phenotype, non-enhanceable by Btk^k00206

(Jackson and Berg, 1999)

ct^C145 has phenotype, non-enhanceable by Egfr^f24

(Jackson and Berg, 1999)

ct^C145 has phenotype, non-enhanceable by Src64B^Δ17

(Jackson and Berg, 1999)

ct^C145 has phenotype, non-enhanceable by arm¹

(Jackson and Berg, 1999)

ct^C145 has phenotype, non-enhanceable by arm⁴

(Jackson and Berg, 1999)

ct^C145 has phenotype, non-enhanceable by chic[+]/chic^k13321

(Jackson and Berg, 1999)

ct^C145 has phenotype, non-enhanceable by chic⁰¹³²⁰

(Jackson and Berg, 1999)

ct^C145 has phenotype, non-enhanceable by chic⁰⁷⁸⁸⁶

(Jackson and Berg, 1999)

ct^C145 has phenotype, non-enhanceable by chic^k13321

(Jackson and Berg, 1999)

ct^C145 has phenotype, non-enhanceable by qua⁹

(Jackson and Berg, 1999)

ct^C145 has phenotype, non-enhanceable by spir¹

(Jackson and Berg, 1999)

ct^C145 has phenotype, non-enhanceable by spir²

(Jackson and Berg, 1999)

ct^C145 has phenotype, non-enhanceable by sqh¹

(Jackson and Berg, 1999)

ct^C145 has phenotype, non-enhanceable by sqh²

(Jackson and Berg, 1999)

ct^C145 has phenotype, non-enhanceable by chic[+]/chic⁰¹³²⁰

(Jackson and Berg, 1999)

ct^C145 has phenotype, non-enhanceable by sqh¹/sqh[+]

(Jackson and Berg, 1999)

ct^C145 has phenotype, non-enhanceable by sqh²/sqh[+]

(Jackson and Berg, 1999)

ct^C145 has phenotype, non-enhanceable by arm¹/arm[+]

(Jackson and Berg, 1999)

ct^C145 has phenotype, non-enhanceable by arm⁴/arm[+]

(Jackson and Berg, 1999)

ct^C145 has phenotype, non-enhanceable by spir[+]/spir¹

(Jackson and Berg, 1999)

ct^C145 has phenotype, non-enhanceable by spir²/spir[+]

(Jackson and Berg, 1999)

Suppressed by

Statement

Reference

ct^C145 has antennal lobe projection neuron vPN | somatic clone phenotype, suppressible by Lim1^UAS.cTa/Scer\GAL4^GH146

(Komiyama and Luo, 2007)

NOT suppressed by

Statement

Reference

ct^C145 has epidermal cell phenotype, non-suppressible by crb^8F105

(Campbell et al., 2009)

Suppressor of

Statement

Reference

ct[+]/ct^C145 is a suppressor of egg chamber phenotype of N^l1N-ts1

(Jackson and Blochlinger, 1997)

ct^C145 is a suppressor of Malpighian tubule phenotype of shg^g317

(Tepass et al., 1996)

Other

Statement

Reference

LIMK1^agn-ts3, ct^C145 has egg chamber phenotype

(Jackson and Berg, 1999)

capu¹, ct^C145 has egg chamber phenotype

(Jackson and Berg, 1999)

capu¹, ct^C145 has nurse cell ring canal phenotype

(Jackson and Berg, 1999)

capu², ct^C145 has egg chamber phenotype

(Jackson and Berg, 1999)

capu², ct^C145 has nurse cell ring canal phenotype

(Jackson and Berg, 1999)

Df(1)sd72b, ct^C145 has wing phenotype

(Jackson and Berg, 1999)

Df(1)A209, ct^C145 has macrochaeta phenotype

(Jackson and Berg, 1999)

capu^HK3, ct^C145 has egg chamber phenotype

(Jackson and Berg, 1999)

Antp², ct^C145 has humeral bristle phenotype

(Johnston et al., 1998)

Antp^73b, ct^C145 has humerus phenotype

(Johnston et al., 1998)

Antp^73b, ct^C145 has dorsal prothorax phenotype

(Johnston et al., 1998)

Antp^CB, ct^C145 has humeral bristle phenotype

(Johnston et al., 1998)

Antp^CB, ct^C145 has humerus phenotype

(Johnston et al., 1998)

Antp^CB, ct^C145 has dorsal prothorax phenotype

(Johnston et al., 1998)

Antp^R, ct^C145 has humeral bristle phenotype

(Johnston et al., 1998)

Antp^R, ct^C145 has humerus phenotype

(Johnston et al., 1998)

Antp^R, ct^C145 has dorsal prothorax phenotype

(Johnston et al., 1998)

Antp², ct^C145 has humerus phenotype

(Johnston et al., 1998)

Antp^Wu, ct^C145 has humeral bristle phenotype

(Johnston et al., 1998)

Antp^Wu, ct^C145 has humerus phenotype

(Johnston et al., 1998)

Antp^Wu, ct^C145 has dorsal prothorax phenotype

(Johnston et al., 1998)

Antp², ct^C145 has dorsal prothorax phenotype

(Johnston et al., 1998)

Antp²⁵, ct^C145 has humeral bristle phenotype

(Johnston et al., 1998)

Antp¹¹, ct^C145 has humeral bristle phenotype

(Johnston et al., 1998)

Antp²⁵, ct^C145 has humerus phenotype

(Johnston et al., 1998)

Antp¹¹, ct^C145 has humerus phenotype

(Johnston et al., 1998)

Antp¹¹, ct^C145 has dorsal prothorax phenotype

(Johnston et al., 1998)

Antp¹⁶, ct^C145 has humeral bristle phenotype

(Johnston et al., 1998)

Antp¹⁶, ct^C145 has humerus phenotype

(Johnston et al., 1998)

Antp¹⁶, ct^C145 has dorsal prothorax phenotype

(Johnston et al., 1998)

Antp²⁵, ct^C145 has dorsal prothorax phenotype

(Johnston et al., 1998)

Antp²², ct^C145 has humeral bristle phenotype

(Johnston et al., 1998)

Antp²², ct^C145 has humerus phenotype

(Johnston et al., 1998)

Antp²², ct^C145 has dorsal prothorax phenotype

(Johnston et al., 1998)

Antp¹¹, ct^L188/ct^C145 has humeral bristle phenotype

(Johnston et al., 1998)

Antp¹¹, ct^L188/ct^C145 has humerus phenotype

(Johnston et al., 1998)

Antp¹¹, ct^L188/ct^C145 has dorsal prothorax phenotype

(Johnston et al., 1998)

Antp^73b, ct^C145 has humeral bristle phenotype

(Johnston et al., 1998)

Polr2B^wimp, ct^C145 has germline cyst phenotype

(Jackson and Blochlinger, 1997)

Polr2B^wimp, ct^C145 has egg chamber phenotype

(Jackson and Blochlinger, 1997)

Polr2B^wimp, ct^C145 has germline cell | female phenotype

(Jackson and Blochlinger, 1997)

Additional Comments

Genetic Interactions

Statement

Reference

Tubules in ct^C145; crb¹ double-mutant embryos resemble those of ct^C145 single mutants; they form epithelial blisters.

(Campbell et al., 2009)

The transformation of arista to leg seen in flies carrying antennal ct^C145 clones is enhanced if they also carry ss^a; both the severity of the transformation and the percentage of flies showing the transformation is increased in the double mutants.

(Ebacher et al., 2007)

Lim1^Scer\UAS.cTa; Scer\GAL4^GH146 does not suppress the reduction in ventral antennal lobe projection neuron (vPN) numbers seen in ct^C145/ct^C145 somatic clones but does partially rescue the defects in targeting to antennal glomeruli seen in these neurons. Targeting defects in lateral antennal lobe projection neurons (lPN) in these clones are not rescued by Lim1^Scer\UAS.cTa; Scer\GAL4^GH146.

(Komiyama and Luo, 2007)

ct^C145/+ ; bft⁶/bft⁶ animals do not survive to adulthood.

(Hardiman et al., 2002)

ct^C145/+ ; capu¹/+ and ct^C145/+ ; capu²/+ double heterozygotes produce egg chambers with binucleate cells. The majority of egg chambers contain a single binucleate cell, although occasionally more than one binucleate cell per egg chamber is seen. The binucleate cells can occur anywhere among the nurse cells and contain remnants of ring canals. The binucleate cells are not seen prior to stage 5. ct^C145 produces egg chambers with binucleate cells in double heterozygous combination with a number of deficiencies; Df(1)JC70, Df(1)RA2, Df(1)KA14, Df(1)N105, Df(1)JA26, Df(2L)30A-C, Df(2R)44CE, Df(2R)eve, Df(2R)or-BR6, Df(2R)M60E, Df(3L)GN50, Df(3L)GN24, Df(3L)66C-G28, Df(3L)AC1, Df(3L)W4, Df(3R)Antp17, Df(3R)P14, Df(1)otu-PΔ1 and Df(3R)Tl-P. capu^HK3 does not interact with ct^C145 in a doubly heterozygous background, although it does enhance the frequency of binucleate cell production in the egg chambers of ct^C145/ct^L188 animals. Src64B^Δ17, qua⁹, Egfr^f24, Btk29A^k00206, spir¹, spir², arm⁴/+, chic⁰⁷⁸⁸⁶/+ or chic^k13321/+ do not interact with ct^C145/ct^L188. Dominantly enhances the wing notching phenotype seen in Df(1)N-8/+ flies; notches are deeper and more frequent. Double heterozygotes with Df(1)sd72b show a wing notching phenotype. ct^C145/Df(1)A209 flies have shortened and tapered bristles. ct^C145/+ ; otu¹¹/+ egg chambers contain binucleate cells. The majority of egg chambers contain a single binucleate cell, which can be positioned anywhere in the egg chamber, although occasionally more than one binucleate cell per egg chamber is seen. ct^C145/agn¹ females placed at the restrictive temperature (29^oC) for 5 days have egg chambers which contain binucleate cells (1-5% of all egg chambers).

(Jackson and Berg, 1999)

63% of ct^L188/ct^C145; Antp¹¹/+ flies show a humeral outgrowth phenotype at 24^oC.

(Johnston et al., 1998)

Egg chambers of ct^L188/ct^C145 females sometimes contain two diploid nuclei, and the distribution of ring canals may be abnormal. Ovaries from ct^C145/+ ; RpII140^wimp/+ females contain egg chambers with an abnormal number of germline cells and show cyst encapsulation defects. No multinucleate cells are seen in the egg chambers.

(Jackson and Blochlinger, 1997)

Malpighian tubule defect of shg^g317 is rescued by ct^C145.

(Tepass et al., 1996)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

ct^lS2

(Liu et al., 1991)

ct^L242

(Liu et al., 1991)

ct^L221

(Liu et al., 1991)

Partially rescued by

ct^C145 is partially rescued by ct^UAS.cPa/Scer\GAL4^GH146

(Komiyama and Luo, 2007)

Comments

Images (0)

Mutant

Wild-type

Stocks (2)

Bloomington

6946

y¹ w¹ ct^C145/FM3/Dp(1;Y)ct⁺y⁺

36496

w^* ct^C145 P{neoFRT}19A/FM7c; P{UAS-ct.P}2, P{UAS-mCD8::GFP.L}LL5/CyO

Notes on Origin

Discoverer

Lefevre.

Comments

lethal II cut phenotypic class.

(Blochlinger et al., 1990)

A cut lethal II phenotypic class allele. ct^C145 failed to complement ct^lS2, ct^L188, ct^L221 and ct^L242.

(Liu et al., 1991)

Germline clonal analysis indicates that ct function is not required in the germline during oogenesis.

(Jackson and Blochlinger, 1997)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (6)

Reported As

Symbol Synonym

ct¹⁴⁵

(Xu et al., 2018, Levine et al., 2010, Emerald et al., 2003, Vervoort et al., 1995, Couso et al., 1994)

ct^C145

(Plavicki et al., 2012, Wang and Sun, 2012)

ct^c145

(Bhattacharjee et al., 2023, Iyer et al., 2013, Olesnicky et al., 2012, Campbell et al., 2009, Ebacher et al., 2007, Jinushi-Nakao et al., 2007, Li et al., 2004, Sugimura et al., 2004, Grueber et al., 2003, Hardiman et al., 2002)

cut¹⁴⁵

(Tsikala et al., 2014, Duncan et al., 2010, Kim et al., 2006, Canon and Banerjee, 2003)

cut^C145

(Xu et al., 2018, Becam et al., 2011, Komiyama and Luo, 2007, Jarman and Ahmed, 1998)

cut^c145

(Arya et al., 2019, Lyons et al., 2014, Levine et al., 2010, Long et al., 2009)

Name Synonyms

cutC145

(Lin et al., 2011)

Secondary FlyBase IDs

References (50)

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