FlyBase Allele Report: Dmel\pros[17]

When the majority of eye cells are homozygous pros¹⁷ mutant using Minute clones, the corneal lenses display slightly irregular shapes and sizes compared with wild-type eyes.

(Charlton-Perkins et al., 2011)

Most homozygous neuroblast clones in the larval brain are significantly larger than control clones. The mutant clones contain an increased number of mitotically active cells compared to controls. Two main types of neuroblast clone are recovered in the central brain. Clones of the first type (3 times more common than the second type) are larger than control clones, but are similar to them in that they contain one or two large cells located on one side of the cluster which seem to correspond to the neuroblast and/or ganglion mother cell. These clones also contain several small BrdU labelled nuclei. Mutant clones of the second type are very large and mostly contain large-to-medium size cells that are scattered throughout the clone. Two comparable types of mutant clone are recovered in the outer proliferation centre, with the first type of clone being 4 times more common than the second type.

(Colonques et al., 2011)

Homozygous clones induced by the eyFLP method result in ectopic CO[[2]] neurons on the maxillary palp (MP). The ectopic neurons show dual targeting specificity: in addition to targeting the V-glomerulus they also innervate a set of medial glomeruli normally innervated by two MP olfactory receptor neuron classes. The number of antennal CO[[2]] neurons is reduced to 51.5% of controls. The number of olfactory receptor neurons per maxillary palp is reduced.

(Hartl et al., 2011)

pros¹⁷ type I neuroblast clones in the larval brain contain ectopic type I neuroblasts. In contrast, pros¹⁷ type II neuroblast clones accumulate ectopic Intermediate Neural Progenitors while maintaining single parental neuroblasts.

(Weng et al., 2010)

62% of individual pros¹⁷ mutant R7 cells (generated using MARCM) form synaptic boutons in both the R7 and R8 medullar layers.

(Miller et al., 2008)

In third instar larvae, pros¹⁷ mutant clones appear to have increased in size and be populating large areas of the central brain compared to wild-type controls. Over 90% of pros¹⁷ clones contain 200-1000 cells compared to <100 cells in wild-type clones.

(Bello et al., 2006)

The morphology of the CNS is severely impaired in pros¹⁷ stage 15 embryos. The RP2, aCC/pCC and U/CQ neurons are missing but the EL neuron cluster is not affected.

pros¹⁷ neuroblast clones overproliferate when generated in the posterior half of the larval brain. Tumours are also formed when clones are induced in the ventral nerve cord. The neuroblasts within the tumours are enlarged.

(Betschinger et al., 2006)

Whereas wild type neuroblasts generate 2-32 cells (average 16.2 cells) and most exhibit extensive axonal outgrowth, pros¹⁷ neuroblasts generate 8-51 cells (average 31.8 cells) and exhibit few if any projections, and the cells are smaller in size.

Whereas wild type ganglion mother cells (GMCs) consistently give rise to just 2 daughter cells, which extend axons, pros¹⁷ GMCs give rise to more than 2 daughter cells, which exhibit few if any signs of differentiation, rarely producing projections.

(Choksi et al., 2006)

pros¹⁷ mutant clones fails to differentiate ganglion mother cells.

(Lee et al., 2006)

The transplantation of pros¹⁷ larval neuroblast clones into the abdomen of adult hosts causes tumor growth, with clones growing to 100 times their original size thereby severely damaging and displacing the host's organs. Although genome stability is not grossly affected shortly after transplantation, 40-day-old tumors show karyotype defects such as segmental aneuploidy. Additionally, 15-20% of cells within the tumors have supernumerary centrosomes and these cells tend to be hyperploid.

(Caussinus and Gonzalez, 2005)

Only 5% of hemisegments in pros¹⁷ mutant embryos have an RP2 neuron/RP2 neuron sib pair. However, there is no imbalance in the RP2/sib ratio in any segments. There is also a reduction in numbers U and CQ lineage neurons per segment (some segments lack neurons all together).

(Bhat and Apsel, 2004)

Glial cell fragmentation occurs in sensory organ clusters of the microchaete lineage of the notum in homozygous clones (as occurs in wild type).

(Fichelson and Gho, 2003)

When homozygous somatic clones are made in the antenna, various defects are seen. Sensillae are seen with duplicated shafts or sockets. Occasionally three shafts are seen arising from a single socket.

(Sen et al., 2003)

Mutant embryos show a striking loss of NGB 6-4T derived glia. The progeny of the G daughter cell of NGB 6-4T fail to migrate to the midline. These progeny cells fail to express either glial or neuron specific markers suggesting that they are unable to differentiate as glia or neurons. Mutant embryos also show defects in glial cell fate in the NGB 7-4 lineage.

(Freeman and Doe, 2001)

In pros¹⁷ mutants the differentiation of the NGB6-4T-derived glial cells is abnormal. the M-CBG and two MM-CBGs are absent.

(Ragone et al., 2001)

Mutants show no repo-positive cells of the NB6-4T or NB7-4 lineage. NB6-4T produces the normal number of progeny but none adopt the glial fate, all remaining in the neuronal, lateral position. NB6-4A is not affected by pros mutants.

(Akiyama-Oda et al., 2000)

Mutant embryos show a continuous decrease in myopodia number throughout hours 13-16, with only 2.23 myopodia per muscle remaining at hour 16. Whereas hour 16 wild type muscles show myopodia clustering in 46 of 52 hemisegments examined, pros¹⁷ show only 3 of 21 muscle cells with regions of high myopodial density.

(Ritzenthaler et al., 2000)

Defects in dentritic misrouting are seen in embryos. No obvious cell change is seen in the PNS, but abnormal outgrowth and misrouting of axons from dorsal clusters of sensory neurons is seen. Dorsal branches may cross each other or veer sharply toward the other dorsal branch, unlike wild-type, where dorsal branches stay clear of each other. These sorts of phenotype are seen in about 70% of embryos.

(Gao et al., 1999)

Homozygous clones in the notum contain 86% single bristles (wild type) and 14% double bristles (two bristle shafts emerging from a single or fused double socket) in females. Males also show double bristles but at lower frequency. Homozygous clones in the eye contain 46% single bristles and 54% double bristles. The double bristle sense organs usually contain one morphologically normal bristle and one stunted bristle. The axon of the neuron is stunted in single bristle sense organs and often has a circular trajectory, and the dendrite is extremely stunted and usually fails to connect with the base of the bristle/socket cells.

(Manning and Doe, 1999)

Most pros¹⁷ sensilla on the notum and head have the normal complement of external cells (the tormogen and trichogen). The neuronal cells lying beneath the sensilla are usually missing in these clones, although in a small number of cases the cell body is present but lacks an apical dendrite. Defects in the external sensory organs are seen in clones; sensory organs with twinned shafts and two sockets, two sockets and a single shaft and two shafts and a single socket are seen. Mechanosensory organs in the eye often show twinning of the shafts, and may also lack the underlying neuron.

(Reddy and Rodrigues, 1999)

Peripheral glia are present in embryos, but do not extend cytoplasmic processes. The thoracic intersegmental glia and midline glia are abnormally large.

(Nelson and Laughon, 1994)

Haploinsufficiency for Abl, loss of one gene copy of pros exacerbates the Abl^- mutant phenotype.

(Gertler et al., 1993)

Lack longitudinal tracts and glial differentiation stops at a pre-axonal stage.

(Jacobs, 1993)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

Chro⁷¹/Chro⁶¹², pros[+]/pros¹⁷ has decreased occurrence of cell division | third instar larval stage phenotype, suppressible | partially by Scer\GAL4^insc-Mz1407/grh^UAS.cUa

(Li et al., 2017)

NOT suppressed by

Statement

Reference

pros¹⁷ has abnormal neuroanatomy | somatic clone phenotype, non-suppressible by Scer\GAL4^elav-C155/erm^UAS.Tag:HA

(Weng et al., 2010)

Enhancer of

Statement

Reference

pros¹⁷ is an enhancer of abnormal neurophysiology | adult stage phenotype of Hsap\MAPT^{P301L.QUAS.0N4R}, Ncra\QF^QF2w.nSyb

(Praschberger et al., 2023)

pros[+]/pros¹⁷ is an enhancer of visible | adult stage phenotype of Hsap\ABL1::Hsap\BCR^UAS.cBa, Scer\GAL4^GMR.PU

(Bernardoni et al., 2019)

pros¹⁷ is an enhancer of abnormal neuroanatomy | embryonic stage phenotype of kuz^e29-4

(Ulvklo et al., 2012)

pros¹⁷ is an enhancer of increased cell number | embryonic stage phenotype of kuz^e29-4

(Ulvklo et al., 2012)

pros¹⁷ is an enhancer of decreased cell number | embryonic stage | maternal effect phenotype of brat^2L-150-11

(Betschinger et al., 2006)

pros¹⁷ is an enhancer of abnormal neuroanatomy phenotype of brat^2L-150-11

(Betschinger et al., 2006)

NOT Enhancer of

Statement

Reference

pros[+]/pros¹⁷ is a non-enhancer of abnormal neuroanatomy | larval stage phenotype of N^{UAS.Tag:V5,Tag:polyHis}, Scer\GAL4^insc-Mz1407, mir-ban^{sponge.UAS.DsRed(Unk)}

(Wu et al., 2017)

pros[+]/pros¹⁷ is a non-enhancer of increased cell number | larval stage phenotype of N^{UAS.Tag:V5,Tag:polyHis}, Scer\GAL4^insc-Mz1407, mir-ban^{sponge.UAS.DsRed(Unk)}

(Wu et al., 2017)

Suppressor of

Statement

Reference

pros¹⁷ is a suppressor | partially of decreased occurrence of cell division | larval stage phenotype of Scer\GAL4^insc-Mz1407, kin17^HMC03906

(Connell et al., 2024)

pros¹⁷ is a suppressor | partially of decreased size | larval stage phenotype of Scer\GAL4^insc-Mz1407, kin17^HMC03906

(Connell et al., 2024)

pros¹⁷ is a suppressor | partially of decreased cell number | larval stage phenotype of Scer\GAL4^insc-Mz1407, kin17^HMC03906

(Connell et al., 2024)

pros[+]/pros¹⁷ is a suppressor of abnormal neuroanatomy | larval stage phenotype of Scer\GAL4^pnt-14-94, Six4^{UAS.ORF.GW.Tag:HA}

(Chen et al., 2021)

pros[+]/pros¹⁷ is a suppressor of decreased cell number | larval stage phenotype of Scer\GAL4^pnt-14-94, Six4^{UAS.ORF.GW.Tag:HA}

(Chen et al., 2021)

pros[+]/pros¹⁷ is a suppressor | partially of decreased occurrence of cell division | third instar larval stage phenotype of Chro⁷¹/Chro⁶¹², Scer\GAL4^insc-Mz1407, grh^UAS.cUa

(Li et al., 2017)

pros[+]/pros¹⁷ is a suppressor | partially of decreased occurrence of cell division | somatic clone phenotype of Mgtor^k03905

(Li et al., 2017)

pros[+]/pros¹⁷ is a suppressor | partially of decreased occurrence of cell division | third instar larval stage phenotype of Chro⁷¹/Chro⁶¹²

(Li et al., 2017)

pros[+]/pros¹⁷ is a suppressor | partially of decreased cell number | third instar larval stage phenotype of Scer\GAL4^pnt-14-94, pnt^HMS01452

(Xie et al., 2016)

pros[+]/pros¹⁷ is a suppressor | partially of abnormal neuroanatomy | third instar larval stage phenotype of Scer\GAL4^pnt-14-94, pnt^HMS01452

(Xie et al., 2016)

NOT Suppressor of

Statement

Reference

pros[+]/pros¹⁷ is a non-suppressor of abnormal neuroanatomy | larval stage phenotype of N^{UAS.Tag:V5,Tag:polyHis}, Scer\GAL4^insc-Mz1407, mir-ban^{sponge.UAS.DsRed(Unk)}

(Wu et al., 2017)

pros[+]/pros¹⁷ is a non-suppressor of increased cell number | larval stage phenotype of N^{UAS.Tag:V5,Tag:polyHis}, Scer\GAL4^insc-Mz1407, mir-ban^{sponge.UAS.DsRed(Unk)}

(Wu et al., 2017)

Other

Statement

Reference

pros[+]/pros¹⁷, wts^x1 has abnormal neuroanatomy | embryonic stage phenotype

(Keder et al., 2015)

pros¹⁷, trx^unspecified has abnormal neuroanatomy | somatic clone | larval stage phenotype

(Komori et al., 2014)

pros¹⁷, tll^l49 has abnormal neuroanatomy phenotype

(Kurusu et al., 2009)

glu^k08819, pros¹⁷ has abnormal mitotic cell cycle phenotype

(Cobbe et al., 2006)

Phenotype Manifest In

Suppressed by

Statement

Reference

Chro⁷¹/Chro⁶¹², pros[+]/pros¹⁷ has neuroblast | third instar larval stage phenotype, suppressible | partially by Scer\GAL4^insc-Mz1407/grh^UAS.cUa

(Li et al., 2017)

NOT suppressed by

Statement

Reference

pros¹⁷ has larval neuroblast | ectopic | somatic clone phenotype, non-suppressible by Scer\GAL4^elav-C155/erm^UAS.Tag:HA

(Weng et al., 2010)

Enhancer of

Statement

Reference

pros¹⁷ is an enhancer of retina | adult stage phenotype of Hsap\MAPT^{P301L.QUAS.0N4R}, Ncra\QF^QF2w.nSyb

(Praschberger et al., 2023)

pros[+]/pros¹⁷ is an enhancer of eye phenotype of Hsap\ABL1::Hsap\BCR^UAS.cBa, Scer\GAL4^GMR.PU

(Bernardoni et al., 2019)

pros¹⁷ is an enhancer of apterous-expressing neuron of the lateral cluster of the thorax phenotype of kuz^e29-4

(Ulvklo et al., 2012)

pros[+]/pros¹⁷ is an enhancer of lens | somatic clone phenotype of sv^spa-pol

(Charlton-Perkins et al., 2011)

pros¹⁷ is an enhancer of cone cell | somatic clone phenotype of sv^spa-pol

(Charlton-Perkins et al., 2011)

NOT Enhancer of

Statement

Reference

pros[+]/pros¹⁷ is a non-enhancer of type II neuroblast | larval stage | increased number phenotype of N^{UAS.Tag:V5,Tag:polyHis}, Scer\GAL4^insc-Mz1407, mir-ban^{sponge.UAS.DsRed(Unk)}

(Wu et al., 2017)

Suppressor of

Statement

Reference

pros¹⁷ is a suppressor | partially of larval brain | larval stage phenotype of Scer\GAL4^insc-Mz1407, kin17^HMC03906

(Connell et al., 2024)

pros¹⁷ is a suppressor | partially of ganglion mother cell | larval stage | decreased number phenotype of Scer\GAL4^insc-Mz1407, kin17^HMC03906

(Connell et al., 2024)

pros[+]/pros¹⁷ is a suppressor of larval brain | larval stage phenotype of Scer\GAL4^pnt-14-94, Six4^{UAS.ORF.GW.Tag:HA}

(Chen et al., 2021)

pros[+]/pros¹⁷ is a suppressor of type II neuroblast | increased number | larval stage phenotype of Scer\GAL4^pnt-14-94, Six4^{UAS.ORF.GW.Tag:HA}

(Chen et al., 2021)

pros[+]/pros¹⁷ is a suppressor of intermediate neuronal progenitor | larval stage | decreased number phenotype of Scer\GAL4^pnt-14-94, Six4^{UAS.ORF.GW.Tag:HA}

(Chen et al., 2021)

pros[+]/pros¹⁷ is a suppressor | partially of neuroblast | third instar larval stage phenotype of Chro⁷¹/Chro⁶¹²

(Li et al., 2017)

pros[+]/pros¹⁷ is a suppressor | partially of neuroblast | third instar larval stage phenotype of Chro⁷¹/Chro^17a

(Li et al., 2017)

pros[+]/pros¹⁷ is a suppressor | partially of neuroblast | third instar larval stage phenotype of Chro⁷¹/Chro^8c

(Li et al., 2017)

pros[+]/pros¹⁷ is a suppressor | partially of neuroblast | third instar larval stage phenotype of Chro⁷¹/Chro⁶¹², Scer\GAL4^insc-Mz1407, grh^UAS.cUa

(Li et al., 2017)

pros[+]/pros¹⁷ is a suppressor | partially of neuroblast | somatic clone | third instar larval stage phenotype of Mgtor^k03905

(Li et al., 2017)

pros[+]/pros¹⁷ is a suppressor | partially of intermediate neuronal progenitor | third instar larval stage phenotype of Scer\GAL4^pnt-14-94, pnt^HMS01452

(Xie et al., 2016)

pros[+]/pros¹⁷ is a suppressor | partially of type II neuroblast | third instar larval stage phenotype of Scer\GAL4^pnt-14-94, pnt^HMS01452

(Xie et al., 2016)

NOT Suppressor of

Statement

Reference

pros[+]/pros¹⁷ is a non-suppressor of type II neuroblast | increased number | larval stage phenotype of N^{UAS.Tag:V5,Tag:polyHis}, Scer\GAL4^insc-Mz1407, mir-ban^{sponge.UAS.DsRed(Unk)}

(Wu et al., 2017)

Other

Statement

Reference

pros[+]/pros¹⁷, wts^x1 has larval RP2 motor neuron | embryonic stage phenotype

(Keder et al., 2015)

pros¹⁷, trx^unspecified has type I neuroblast | increased number | somatic clone | larval stage phenotype

(Komori et al., 2014)

kuz^e29-4, pros¹⁷ has larval thoracic NB5-6 primary interneuron phenotype

(Ulvklo et al., 2012)

brat^2L-150-11, pros¹⁷ has axon phenotype

(Betschinger et al., 2006)

brat^2L-150-11, pros¹⁷ has larval EL neuron phenotype

(Betschinger et al., 2006)

glu^k08819, pros¹⁷ has mitosis & nuclear chromosome phenotype

(Cobbe et al., 2006)

Rh6¹, pros¹⁷ has photoreceptor cell R7 phenotype

(Cook et al., 2003)

Rh6¹, pros¹⁷ has photoreceptor cell R8 | ectopic phenotype

(Cook et al., 2003)

Additional Comments

Genetic Interactions

Statement

Reference

The central brain neuroblast reactivation defects (manifested by the retention of cellular extensions and low mitotic activity even at late larval stages) characteristic for Chro⁷¹/Chro⁶¹² mutants are alleviated by combination with a single copy of pros¹⁷, the phenotype can be further improved when grh^Scer\UAS.cUa is expressed under the control of Scer\GAL4^insc-Mz1407 in the Chro⁷¹/Chro⁶¹²;pros¹⁷/+ mutant background.

The reactivation defects observed in central neuroblast Mtor^k03905 MARCM mutant clones are partially rescued by single copy of pros¹⁷.

(Li et al., 2017)

The presence of pros¹⁷/+ does not change the number of neuroblasts per brain lobe seen in larval brains expressing both ban^{sponge.Scer\UAS.T:Disc\RFP} and N^{Scer\UAS.T:SV5\V5,T:Zzzz\His6} under the control of Scer\GAL4^insc-Mz1407.

(Wu et al., 2017)

pros¹⁷/+ partially suppresses the loss of intermediate neural progenitors and Asense-negative neuroblasts seen in larvae expressing pnt^HMS01452 under the control of Scer\GAL4^pnt-14-94.

(Xie et al., 2016)

The proportion of hemisegments with abnormal number of neurons in the asymmetrically dividing RP2 neural lineage is significantly increased in wts^x1/+;pros¹⁷/+ double heterozygous embryos compared to either of the single heterozygotes or wild type.

(Keder et al., 2015)

trx^unspecified pros¹⁷ double mutant type II neuroblast clones form supernumerary type I neuroblasts.

(Komori et al., 2014)

kuz^e29-4 ; pros¹⁷ double mutant embryos show extensive overproliferation of the entire NB5-6T lineage, with an average of 69 cells. There is an increase in the number of "Ap" neurons generated in the NB5-6T lineage in the double mutant embryos compared to kuz^e29-4 single mutant embryos.

(Ulvklo et al., 2012)

pros¹⁷ mutants that are also heterozygous for pros¹⁷ show a much more severe lens phenotype than either individual mutant, with many ommatidia having reduced, defective, or missing lenses. These mutants also display a reduced number of cone cells per ommatidia.

Lens structures are missing in pros¹⁷, sv^spa-pol double mutants. No cone cells are detected in these mutants.

(Charlton-Perkins et al., 2011)

Overexpression of erm^{Scer\UAS.T:Ivir\HA} under the control of Scer\GAL4^elav-C155 fails to suppress ectopic Intermediate Neural Progenitors in pros¹⁷ mutant type II neuroblast clones in the larval brain.

(Weng et al., 2010)

In brat^2L-150-11, pros¹⁷ mutant embryos, the CNS phenotype is enhanced compared to either single mutant. In addition to the loss of neurons seen in the single mutants, the EL neurons are missing and there is a severe reduction in axon formation.

(Betschinger et al., 2006)

glu^k08819; pros¹⁷ mitotic cells accumulate in prophase/premetaphase. These cells delay in metaphase and display a high frequency of anaphase and telophase bridges.

(Cobbe et al., 2006)

R7 photoreceptors cells homozygous for pros¹⁷ and Rh6¹ undergo partial transformation towards an R8 photoreceptor fate, as judged by marker analysis, mapping of axonal projections, and proximo-distal positioning of nuclei.

(Cook et al., 2003)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

pros^V17

(Grosjean et al., 2003)

Comments

Images (0)

Mutant

Wild-type

Stocks (2)

Bloomington

5458

w^*; pros¹⁷/TM6B, Tb¹

Kyoto

108250

w^*; pros¹⁷/TM6B, Tb¹

Notes on Origin

Discoverer

Comments

FlyBase curator comment: the authors use the symbol "pros[v17]" for the "pros[17]" allele.

(Colonques et al., 2011)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (5)

Reported As

Symbol Synonym

Pros¹⁷

(Tripathi et al., 2017)

pros17

(Shen et al., 1997)

pros¹⁷

(Connell et al., 2024, Nguyen and Cheng, 2024, An et al., 2023, Praschberger et al., 2023, Wu et al., 2023, Mar et al., 2022, Avetisyan et al., 2021, Chen et al., 2021, Hatch et al., 2021, Liu et al., 2020, Bernardoni et al., 2019, Jia et al., 2019, Shaw et al., 2018, Li et al., 2017, Liu et al., 2017, Sallé et al., 2017, Wu et al., 2017, Narbonne-Reveau et al., 2016, Xie et al., 2016, Keder et al., 2015, Weng and Cohen, 2015, Zeng and Hou, 2015, Baumgardt et al., 2014, Komori et al., 2014, Lai and Doe, 2014, Xie et al., 2014, Chai et al., 2013, Ulvklo et al., 2012, Charlton-Perkins et al., 2011, Hartl et al., 2011, Kuzin et al., 2011, Berger et al., 2010, Janic et al., 2010, Weng et al., 2010, Andrews et al., 2009, Kurusu et al., 2009, Sousa-Nunes et al., 2009, Miller et al., 2008, Bello et al., 2006, Betschinger et al., 2006, Choksi et al., 2006, Cook, 2006.10.1, Lee et al., 2006, Lee et al., 2006, Caussinus and Gonzalez, 2005, Grosjean et al., 2003)

pros^17e

(Ritzenthaler et al., 2000)

prospero¹⁷

(Grosskortenhaus et al., 2005)

Name Synonyms

prospero17

(Ganesan et al., 2011, Choksi et al., 2006)

Secondary FlyBase IDs

References (77)

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