Allele Dmel\tutl⁰¹⁰⁸⁵

General Information
Symbol	Dmel\tutl⁰¹⁰⁸⁵	Species	D. melanogaster
Name		FlyBase ID	FBal0007959
Feature type	allele	Associated gene	Dmel\tutl
Also Known As	l(2)01085

Map ( GBrowse )	Untitled Document
Allele class	hypomorphic allele - genetic evidence
Mutagen	P-element activity
Recent Updates
Description	What does this section display? This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms). What does this section not display? This section does not currently display links that were removed or gene model changes.
Update Feed	Click the icon below to subscribe to this FlyBase record and receive updates automatically through your feed reader.
FB2013_03
FB2013_02
All updates	Click here to see a list of all updates to this record from FB2010_08 and on.
Nature of the Allele
Allele class	hypomorphic allele - genetic evidence (Bodily et al., 2001)
Mutagen	P-element activity
Mutations Mapped to the Genome

Type Location Additional Notes References transposable element insertion site 2L:4,303,444..4,303,444 (BDGP Project Members, 1994-1999, Spradling et al., 1999, Misra, 2000.8.25, Bodily et al., 2001, Al-Anzi and Wyman, 2009, Ferguson et al., 2009, Vicente-Crespo et al., 2008)
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference P{PZ} insertion within exon 4, disrupting translation downstream of exon 4. (Bodily et al., 2001) P{PZ} insertion in exon 6 of the CT35488 transcript of tutl, 20251bp downstream of the 5' end of the transcript. (Misra, 2000.8.25)
Caused by insertion	P{PZ}tutl⁰¹⁰⁸⁵ (BDGP Project Members, 1994-1999, Spradling et al., 1999, Misra, 2000.8.25, Bodily et al., 2001, Al-Anzi and Wyman, 2009, Ferguson et al., 2009, Vicente-Crespo et al., 2008)
Cytology
Phenotypic Data
Phenotypic Class
	behavior defective \| larval stage (with Df(2L)tutl⁴) (Bodily et al., 2001) behavior defective \| larval stage \| recessive (Bodily et al., 2001) lethal \| recessive (BDGP Project Members, 1994-1999, Bodily et al., 2001, Spradling et al., 1999) neuroanatomy defective (Al-Anzi and Wyman, 2009) neuroanatomy defective (with Df(2L)ed-dp) (Long et al., 2009) neuroanatomy defective (with tutl²³) (Long et al., 2009) neuroanatomy defective (with tutl^ex383) (Al-Anzi and Wyman, 2009) neuroanatomy defective \| somatic clone (Ferguson et al., 2009)
Phenotype Manifest In
	dendrite & dorsal multidendritic neuron ddaC (with tutl²³) (Long et al., 2009) dendrite & dorsal multidendritic neuron ddaE (with Df(2L)ed-dp) (Long et al., 2009) dendrite & dorsal multidendritic neuron ddaE (with tutl²³) (Long et al., 2009) intermediate longitudinal fascicle (Al-Anzi and Wyman, 2009) intermediate longitudinal fascicle (with tutl^ex383) (Al-Anzi and Wyman, 2009) intersegmental nerve branch ISNb of A1-7 (Al-Anzi and Wyman, 2009) intersegmental nerve branch ISNd of A1-7 (Al-Anzi and Wyman, 2009) lateral longitudinal fascicle (Al-Anzi and Wyman, 2009) lateral longitudinal fascicle (with tutl^ex383) (Al-Anzi and Wyman, 2009) lateral medial fascicle (Al-Anzi and Wyman, 2009) lateral medial fascicle (with tutl^ex383) (Al-Anzi and Wyman, 2009) medial longitudinal fascicle (Al-Anzi and Wyman, 2009) medial longitudinal fascicle (with tutl^ex383) (Al-Anzi and Wyman, 2009) midline crossing tract (Al-Anzi and Wyman, 2009) midline crossing tract (with tutl^ex383) (Al-Anzi and Wyman, 2009) photoreceptor cell R7 \| somatic clone (Ferguson et al., 2009) photoreceptor cell R8 \| somatic clone (Ferguson et al., 2009) ventral nerve cord commissure (Al-Anzi and Wyman, 2009) ventral nerve cord commissure (with tutl^ex383) (Al-Anzi and Wyman, 2009)
Detailed Description
	Statement Reference In tutl[01085] embryos, the ISNb motor axons succesfully reach the vicinity of their respective targets. However, once there, many fail to send one or more of the final axon branches to contact their muscle targets. Around a quarter of the hemisegments also lack ISNd nerves. Embryos trans-heterozygous for tutl[ex383] and tutl[01085] have defects in commissures, longitudinal connective, and Fas2-positive axon tracts that maintain their relative distance from the midline, but that have axons emanating from all three fascicles bundle together as they cross the midline. (Al-Anzi and Wyman, 2009) In tutl[01085] eye-specific mosaic animals in which over 90% of R7 and R8 cells are homozygous for tutl[01085], the R7 and R8 axons are disorganised, despite R7 and R8 terminal layers being evident. Many axonal terminals display abnormal lateral extensions and frequently fuse together, particularly at the R7 terminal layer. tutl[01085] mutant R7 and R8 axons from the same ommatidium still associate with each other within the same column. Single tutl[01085] mutant R7 axonal somatic clones display abnormal lateral extension. Compared to wild-type, the frequency of fusion between a labelled tutl[01085] mutant R7 axonal terminal and it's neighbors is increased by approximately 4-10 fold. Among them approximately 53% display a 'U-shape' tiling phenotype, in which a mutant R7 terminal branches out from its column at the R7 recipient layer, extend laterally and fuses with its neighboring R7 terminal. In addition, 47% of terminal fusions display a 'V-shape' phenotype in which a mutant R7 terminal appears to move away from its own column and fuses with its neighboring R7 terminal at the R7 recipient layer. Neighboring wild-type R7 terminals also display a similar degree of tiling defects. Many of them display abnormal lateral extension and frequently extend and fuse with their neighboring R7 terminals, indicating a cell non-autonomous tiling role for tutl between R7 terminals. The majority of defective wild-type R7 axons extend towards their neighboring tutl[01085] mutant axons. In the absence of neighboring R7 terminals, the tendency of a tutl[01085] mutant axon to invade a neighboring column is decreased from approximately 33% for surrounded R7 terminals to approximately 15% for isolated R7 terminals. (Ferguson et al., 2009) Class I ddaE neurons in tutl[01085]/tutl[23] larvae have defects in their dendritic trees, including shortened interstitial branches and curled growth lacking directed orientation. There are also significantly more branch termini per neuron compared to wild type. The number of branch points on primary dendrites is unchanged compared to controls, but there is a clear increase in second and third order branch points in the mutant neurons. tutl[01085]/Df(2L)ed-dp larvae show defects in the dendritic trees of class I ddaE neurons; there are significantly more branch termini per neuron compared to wild type, and although the number of branch points on primary dendrites is unchanged compared to controls, there is a clear increase in second and third order branch points in the mutant neurons. Class IV ddaC neurons in tutl[01085]/tutl[23] larvae show numerous dendrite crossing points, in contrast to control neurons. tutl[01085]/tutl[23] larvae show normal dendritic tiling among class IV da neurons (assayed by examining the borders between ddaC and v'ada neurons for dendritic overlap). (Long et al., 2009) Lethal stage is during mid-eclosion. General morphology of the mutant larvae is normal. Mutant larvae respond to tactile stimulation at their anterior end by contracting at both ends and rocking back and forth in place. After a few seconds of this behaviour, the larvae cease this abnormal movement and return to a normal forward-crawling motion. This contrasts with wild-type larvae which respond by showing a characteristic escape behaviour of 1-3 reverse peristaltic movements followed by a lateral turning behaviour. tutl⁰¹⁰⁸⁵/Df(2L)tutl⁴ larvae have a severely compromised ability to roll over from an inverted position; the time required to right themselves is significantly longer than control larvae. (Bodily et al., 2001)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement Reference tutl⁰¹⁰⁸⁵ has neuroanatomy defective phenotype, enhanceable by Kap-α3^17-76 (Ferguson et al., 2009)
Enhancer of
Statement Reference tutl⁰¹⁰⁸⁵/tutl[+] is an enhancer of neuroanatomy defective phenotype of Kap-α3^17-76 (Ferguson et al., 2009) tutl⁰¹⁰⁸⁵ is an enhancer of neuroanatomy defective phenotype of Actβ^{dsRNA.HL.Scer\UAS}, Scer\GAL4^GMR.long (Ferguson et al., 2009)
NOT Enhancer of
Statement Reference tutl⁰¹⁰⁸⁵/tutl[+] is a non-enhancer of visible \| heat sensitive phenotype of peb¹ (Wilk et al., 2004)
NOT Suppressor of
Statement Reference tutl⁰¹⁰⁸⁵/tutl[+] is a non-suppressor of visible \| heat sensitive phenotype of peb¹ (Wilk et al., 2004)
Phenotype Manifest In
Enhanced by
Statement Reference tutl⁰¹⁰⁸⁵ has photoreceptor cell R7 phenotype, enhanceable by Kap-α3^17-76 (Ferguson et al., 2009)
Enhancer of
Statement Reference tutl⁰¹⁰⁸⁵/tutl[+] is an enhancer of photoreceptor cell R7 phenotype of Kap-α3^17-76 (Ferguson et al., 2009) tutl⁰¹⁰⁸⁵/tutl^k14703 is an enhancer of eye phenotype of Scer\GAL4^hs.2sev, mbl^C.Scer\UAS (Vicente-Crespo et al., 2008) tutl⁰¹⁰⁸⁵ is an enhancer of photoreceptor cell R7 phenotype of Actβ^{dsRNA.HL.Scer\UAS}, Scer\GAL4^GMR.long (Ferguson et al., 2009)
NOT Enhancer of
Statement Reference tutl⁰¹⁰⁸⁵/tutl[+] is a non-enhancer of eye \| heat sensitive phenotype of peb¹ (Wilk et al., 2004)
NOT Suppressor of
Statement Reference tutl⁰¹⁰⁸⁵/tutl[+] is a non-suppressor of eye \| heat sensitive phenotype of peb¹ (Wilk et al., 2004)
Additional Comments
Genetic Interactions
Statement Reference The presence of Actβ[dsRNA.HL.Scer\UAS] in tutl[01085]/+ mutant flies enhances the frequency of fusion between mutant R7 axonal terminals. A tutl[01085] heterozygous background enhances the frequency of tiling defects in Kap-α3[17-76] axonal somatic clones. A Kap-α3[17-76] heterozygous background enhances the frequency of tiling defects in tutl[01085] axonal somatic clones. (Ferguson et al., 2009) A tutl[k14703] ; tutl[01085] mutant background enhances the moderately rough eye phenotype observed upon expression of mbl[C.Scer\UAS] under the control of Scer\GAL4[hs.2sev]. (Vicente-Crespo et al., 2008)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Fails to complement	tutl^k14703 (BDGP Project Members, 1994-1999, Bodily et al., 2001)
Rescued by	tutl⁰¹⁰⁸⁵/tutl²³ is rescued by Scer\GAL4^elav-C155/tutl^Scer\UAS.cLa (Long et al., 2009) tutl⁰¹⁰⁸⁵/tutl²³ is rescued by tutl^Scer\UAS.cLa/Scer\GAL4²²¹ (Long et al., 2009) tutl⁰¹⁰⁸⁵/tutl²³ is rescued by tutl^{Δcyto.Scer\UAS}/Scer\GAL4²²¹ (Long et al., 2009)
Partially rescued by	tutl⁰¹⁰⁸⁵/tutl²³ is partially rescued by Scer\GAL4^elav-C155/tutl^{Δcyto.Scer\UAS} (Long et al., 2009)
Comments
Stocks ( 1 )
Bloomington	10979 P{PZ}tutl⁰¹⁰⁸⁵ cn¹/CyO; ry⁵⁰⁶
Notes on Origin
Discoverer	A. Spradling.

Comments
	Complements: slp1⁰⁵⁹⁶⁵. Complements: l(2)k05819^k05819. Complements: Tps1^k08903. (BDGP Project Members, 1994-1999)
External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 4 )
Reported As
Symbol Synonym	l(2)01085 (Bodily et al., 2001, Misra, 2000.8.25, Spradling et al., 1999) l(2)01085⁰¹⁰⁸⁵ (BDGP Project Members, 1994-1999, ) tutl⁰¹⁰⁸¹ (Wilk et al., 2004) tutl⁰¹⁰⁸⁵ (Jordan et al., 2006, Long et al., 2009, Ferguson et al., 2009)
Name Synonym
Secondary FlyBase IDs

References ( 12 )
Research paper	Al-Anzi and Wyman, 2009, Neural Dev. 4: 31 The Drosophila immunoglobulin gene turtle encodes guidance molecules involved in axon pathfinding. [FBrf0209104] Ferguson et al., 2009, J. Neurosci. 29(45): 14151--14159 The conserved Ig superfamily member turtle mediates axonal tiling in Drosophila. [FBrf0209317] Long et al., 2009, Development 136(20): 3475--3484 Dendrite branching and self-avoidance are controlled by Turtle, a conserved IgSF protein in Drosophila. [FBrf0208798] Vicente-Crespo et al., 2008, PLoS ONE 3(2): e1613 Drosophila muscleblind is involved in troponin T alternative splicing and apoptosis. [FBrf0210274] Jordan et al., 2006, Genetics 174(1): 271--284 Quantitative trait loci for locomotor behavior in Drosophila melanogaster. [FBrf0193517] Wilk et al., 2004, Genetics 168(1): 281--300 Dose-sensitive autosomal modifiers identify candidate genes for tissue autonomous and tissue nonautonomous regulation by the Drosophila nuclear zinc-finger protein, hindsight. [FBrf0180294] Bodily et al., 2001, J. Neurosci. 21(9): 3113--3125 A novel member of the Ig superfamily, turtle, is a CNS-specific protein required for coordinated motor control. [FBrf0135975] Spradling et al., 1999, Genetics 153(1): 135--177 The Berkeley Drosophila genome project gene disruption project. Single P-element insertions mutating 25% of vital Drosophila genes. [FBrf0111489]
Personal communication to FlyBase	Misra, 2000.8.25, nc5 report, second installment. nc5 report, second installment. [FBrf0131112] Beaton, 1999.12.12, Alleles of the lines in the P-element paper. Alleles of the lines in the P-element paper. [FBrf0125032] Meister and Braun, 1995.10, lacZ expression patterns for P{} insertions at Bloomington. lacZ expression patterns for P{} insertions at Bloomington. [FBrf0083714] BDGP Project Members, 1994-1999, BDGP Project Members, 1994-1999, Berkeley Drosophila Genome Project. (Computer file) BDGP Project Members, 1994-1999, Berkeley Drosophila Genome Project. (Computer file) [FBrf0067338]

Allele Dmel\tutl01085

Allele Dmel\tutl⁰¹⁰⁸⁵