Allele Dmel\grim^Scer\UAS.cNa

General Information
Symbol	Dmel\grim^Scer\UAS.cNa	Species	D. melanogaster
Name	Saccharomyces cerevisiae UAS construct a of Nambu	FlyBase ID	FBal0092965
Feature type	allele	Associated gene	Dmel\grim

Allele class
Mutagen	in vitro construct - regulatory fusion
Recent Updates
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FB2013_03
FB2013_02
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Nature of the Allele
Allele class
Mutagen	in vitro construct - regulatory fusion (Chen et al., 1998)
Mutations Mapped to the Genome

Type Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference Construct: Scer\UAS regulatory sequences drive grim expression. (Chen et al., 1998) Scer\UAS sequences drive expression of grim. (Wing et al., 1998)
Carried in construct	P{UAS-grim.N} (Poirier et al., 2008, Sepp et al., 2001, Galindo and Smith, 2001, Seroude, 2002, Wing et al., 2002, Myat and Andrew, 2000, Wing et al., 1998, Wing et al., 2001, Chen et al., 1998, Bauer et al., 2005, Abdou et al., 2011, Brun et al., 2006, Liu et al., 2009, McBrayer et al., 2007, Morris et al., 2006, Rewitz et al., 2009, Niwa et al., 2010, Bidla et al., 2007, Riddiford et al., 2010, Ou et al., 2011)
Cytology
Phenotypic Data
Phenotypic Class
	cell lethal, with Scer\GAL4^Ptth.cMa (McBrayer et al., 2007) cell lethal \| wandering third instar larval stage, with Scer\GAL4^Aug21 (Liu et al., 2009) courtship behavior defective \| male limited, with Scer\GAL4^Ptth.cMa (McBrayer et al., 2007) developmental rate defective, with Scer\GAL4^Ptth.cMa (McBrayer et al., 2007) developmental rate defective \| larval stage, with Scer\GAL4^Aug21 (Riddiford et al., 2010) feeding behavior defective \| second instar larval stage, with Scer\GAL4^sal.BO (Parvy et al., 2012) female semi-fertile, with Scer\GAL4^Ptth.cMa (McBrayer et al., 2007) increased cell death, with Df(3L)H99, Scer\GAL4^Gp150-52A (Wing et al., 1998) increased cell death, with Scer\GAL4^Aug21 (Abdou et al., 2011) increased cell death, with Scer\GAL4^Gp150-52A (Wing et al., 1998) increased cell number, with Scer\GAL4^Ptth.cMa (McBrayer et al., 2007) large body, with Scer\GAL4^Ptth.cMa (McBrayer et al., 2007) lethal, with Scer\GAL4^GMR.PF (Wing et al., 2001, Wing et al., 1998) lethal \| prepupal stage, with Scer\GAL4^Aug21 (Liu et al., 2009, Riddiford et al., 2010) lethal - all die during larval stage, with Scer\GAL4^sal.BO (Parvy et al., 2012) partially lethal - majority die, with Scer\GAL4^Ptth.cMa (McBrayer et al., 2007) short lived, with Scer\GAL4^elav-C155 (Bauer et al., 2005) tarsal response defective, with Scer\GAL4^{Obp57e.T:Hsim\VP16} (Galindo and Smith, 2001)
Phenotype Manifest In
	aCC neuron, with Scer\GAL4^rQ286.11 (Sepp et al., 2001) commissure, with Scer\GAL4^Gp150-52A (Wing et al., 1998) embryonic/larval corpus allatum, with Scer\GAL4^Aug21 (Liu et al., 2009, Riddiford et al., 2010) embryonic/larval fat body \| prepupal stage, with Scer\GAL4^Aug21 (Liu et al., 2009) embryonic/larval glial cell, with Scer\GAL4^repo (Sepp et al., 2001) embryonic/larval glial cell, with Scer\GAL4^rQ286.11 (Sepp et al., 2001) embryonic/larval hemolymph \| third instar larval stage, with Scer\GAL4^He.PZ (Bidla et al., 2007) embryonic/larval nervous system, with Scer\GAL4^rQ286.11 (Sepp et al., 2001) embryonic/larval salivary gland, with Scer\GAL4^Aug21 (Riddiford et al., 2010) embryonic/larval spiracle \| larval stage, with Scer\GAL4^desat1.PB (Parvy et al., 2012) embryonic/larval spiracle \| larval stage, with Scer\GAL4^sal.BO (Parvy et al., 2012) embryonic/larval tracheal system \| larval stage, with Scer\GAL4^sal.BO (Parvy et al., 2012) fat body, with Scer\GAL4^Aug21 (Abdou et al., 2011) midline glial cell, with Df(3L)H99, Scer\GAL4^Gp150-52A (Wing et al., 1998) midline glial cell, with Scer\GAL4^Gp150-52A (Wing et al., 2002, Wing et al., 1998) optic lobe \| prepupal stage, with Scer\GAL4^Aug21 (Riddiford et al., 2010) photoreceptor cell R7 \| prepupal stage, with Scer\GAL4^Aug21 (Riddiford et al., 2010) photoreceptor cell R8 \| prepupal stage, with Scer\GAL4^Aug21 (Riddiford et al., 2010) prothoracic gland innervating neuron PG-LP, with Scer\GAL4^Ptth.cMa (McBrayer et al., 2007) segmental nerve pioneer neuron, with Scer\GAL4^repo (Sepp et al., 2001) segmental nerve pioneer neuron, with Scer\GAL4^rQ286.11 (Sepp et al., 2001) sensory neuron, with Scer\GAL4^repo (Sepp et al., 2001) sensory neuron, with Scer\GAL4^rQ286.11 (Sepp et al., 2001) ventral midline, with Scer\GAL4^Gp150-52A (Wing et al., 2001) ventral nerve cord, with Scer\GAL4^Gp150-52A (Wing et al., 1998) wing, with Scer\GAL4^Ptth.cMa (McBrayer et al., 2007)
Detailed Description
	Statement Reference Expression of grim[Scer\UAS.cNa] under the control of Scer\GAL4[sal.BO] results in lethality at the L2/L3 larval transition. The larvae grow normally until the end of the second instar, but are unable to grow further. They survive a few more days, but eventually contract in size before dying between 4 to 5 days after egg deposition. The larvae often have duplicated mouth hooks of L2 and L3 identity, although some complete the L2/L3 transition. The larvae show abnormal feeding behaviour at the late second instar stage, with more than 50% of the larvae straying away food 1 hour after being placed in a small piece of food in the middle of an agar plate. The tracheal network of animals expressing grim[Scer\UAS.cNa] under the control of Scer\GAL4[sal.BO] appears normally filled with air at the first larval instar stage. However, at the L2/L3 transition the larvae found outside of the food show a severe defect in air-filling of their tracheal trunks. The tubes are still distinguishable, suggesting that they are present but filled with an aqueous solution. The air-filling failure is seen in the spiracles and main trunks, but only occasionally extends into lateral branches and the tracheoles. Larvae expressing grim[Scer\UAS.cNa] under the control of either Scer\GAL4[sal.BO] or Scer\GAL4[desat1.PB] and transferred to blue tinted food medium at the L2 or early L3 stage show blue staining of the spiracles that sometimes extends into the main tracheal trunks, indicating a water-tightness defect in the spiracles. (Parvy et al., 2012) Fat body cells in animals expressing grim[Scer\UAS.cNa] under the control of Scer\GAL4[Aug21] undergo precocious and enhanced programmed cell death compared to wild-type fat body cells. (Abdou et al., 2011) Expression of grim[Scer\UAS.cNa] under the control of Scer\GAL4[Aug21] results in both sets of salivary glands being either missing or in a state of advanced degeneration by the onset of the third larval instar and all remnants of the corpora allata having disappeared by the onset of wandering. Larvae expressing grim[Scer\UAS.cNa] under the control of Scer\GAL4[Aug21] develop slightly more slowly than their control siblings, pupariating about 8-12 hours later (survival to pupariation does not differ between the mutant and control larvae). The mutant pupae are approximately 75% of the weight of their control siblings, although this size defect is rescued if the animals are fed a diet containing 1ppm juvenile hormone mimic during the third instar. Pupae expressing grim[Scer\UAS.cNa] under the control of Scer\GAL4[Aug21] typically die at around the time of head eversion. Head eversion initiates at the normal time, but the mutants are unable to eject the mouth hooks completely and complete head eversion. Escapers that complete head eversion are not found at 29[o]C, but occur in 20% of cases when white puparia are placed at 18[o]C. If the mutant animals are fed a diet containing 1ppm juvenile hormone mimic during the third instar, 89% continue development beyond head eversion and arrest as pharate adults just before eclosion. These pharate adults have truncated and missing abdominal bristles. Animals expressing grim[Scer\UAS.cNa] under the control of Scer\GAL4[Aug21] show a reduction in proliferation in the outer zone of the optic lobe to about 15% of control values by 8 hours after puparium formation. This reduction in mitotic cells can be rescued by feeding on a diet containing juvenile hormone mimic during the larval stage. Proliferation in the inner proliferation zone of the optic lobe also shows a slight, but significant reduction in the mutant prepupae compared to controls, and this can also be rescued by feeding on a diet containing juvenile hormone mimic. Prepupae expressing grim[Scer\UAS.cNa] under the control of Scer\GAL4[Aug21] show precocious separation of the axons of photoreceptors R7 and R8 in the medulla, showing distinct separation by 6 hours after puparium formation. (Riddiford et al., 2010) All of the Scer\GAL4[Aug21]; grim[Scer\UAS.cNa] animals die during early pupal life after normal pupariation. Larval development of Scer\GAL4[Aug21]; grim[Scer\UAS.cNa] animals is delayed and the body weight is reduced. Only about 10% of these pupae undergo successful head eversion. Although the adult organs of these animals initiate development, it is never completed. Internal portions of pupae expressing Scer\GAL4[Aug21]-driven grim[Scer\UAS.cNa] appear to retract progressively from the cuticle (apolysis), creating an apparently empty space beginning 6 hours after pupariation. The fat body in the posterior portion of these pupae often appears to be missing. The fat body in pupae expressing Scer\GAL4[Aug21]-driven grim[Scer\UAS.cNa] undergoes precocious and enhanced programmed cell death and cell dissociation. Cells of the corpus allatum become ablated as a result of Scer\GAL4[Aug21]-driven expression of grim[Scer\UAS.cNa] by early wandering third instar larval stage. jhamt activity is undetectable in wandering third instar larvae expressing grim[Scer\UAS.cNa] driven by Scer\GAL4[Aug21]. In vitro juvenile hormone biosynthesis is undetectable in the brain-ring gland complexes of wandering third instar larvae expressing grim[Scer\UAS.cNa] driven by Scer\GAL4[Aug21]. Methoprene treatment can rescue the lethality of Scer\GAL4[Aug21]-driven expression of grim[Scer\UAS.cNa] in larvae, depending on the dose and of methoprene used and the stage of the larvae treated. The rescued adults are reproductively competent. (Liu et al., 2009) Expression of grim[Scer\UAS.cNa] in the larval hemocytes under the control of Scer\GAL4[He.PZ] results in the formation of melanotic aggregates which contain hemocytes. (Bidla et al., 2007) Larval co-expression of grim[Scer\UAS.cNa] with Scer\GAL4[Ptth.cMa] results in loss of the prothoracic gland (PG) neurons and reduced survival to adulthood. Surviving females show reduced fecundity, while males exhibit male-on-male courtship behaviours. As a result of Scer\GAL4[Ptth.cMa]-driven grim[Scer\UAS.cNa]-expression, wandering third-instar larvae, pupae and adult flies are larger and heavier than wild-type ones. Not only are the bodies of these adults larger and heavier than controls, their wings also show an increase in size due to an increase in cell number. The PG neuron-ablated larvae continue to feed and gain mass for much longer time periods than wild-type controls. The critical weight for pupariation is increased as a result of Scer\GAL4[Ptth.cMa]-driven grim[Scer\UAS.cNa]-overexpression. Scer\GAL4[Ptth.cMa]-driven grim[Scer\UAS.cNa]-expression causes developmental delays. The duration of each larval instar is lengthened in PG neuron ablated animals compared to controls. Not all PG neuron-ablated animals are able to complete development. Different proportion of the Scer\GAL4[Ptth.cMa]-driven grim[Scer\UAS.cNa]-expressing animals die at different stages of larval and pupal development. Dead puparia include elongated prepupae, ones with head-eversion defects, and some with other phenotypes characteristic of reduced ecdyson titers. Larvae expressing Scer\GAL4[Ptth.cMa]-driven grim[Scer\UAS.cNa] show very low ecdysteroid titers throughout the prolonged third-instar stage. As in wild-type, however, an ecdysteroid peak is evident at the white prepupal stage. 20-hydroxyecdysone(20E)-fed, PG neuron-ablated larvae are able to achieve puparium formation 2.5 days after ecdysis to the third instar, whereas controls lacking 20E feeding do not pupariate until 5-6 days. 20E-feeding also restores adult fertility and abnormal larval, pupal and adult size to that of wild-type. (McBrayer et al., 2007) Expression of grim^Scer\UAS.cNa, under the control of Scer\GAL4^elav-C155, shortens the lifespan of flies. (Bauer et al., 2005) Expression of grim^Scer\UAS.cNa under the control of Scer\GAL4^Gp150-52A in embryos in the central nervous system midline results in the loss of some midline glia. (Wing et al., 2002) Expression of grim^Scer\UAS.cNa under the control of Scer\GAL4^{Obp57e.T:Hsim\VP16} results in a dramatic loss of sensitivity to sucrose in a proboscis extension reflex assay. The flies show reduced sensitivity to sucrose compared to wild type at sucrose concentrations from 10^-6 to 10^-2 M, but no significant difference in sensitivity to sucrose compared to wild type at a sucrose concentration of 10^-1 M. (Galindo and Smith, 2001) When grim^Scer\UAS.cNa is driven by Scer\GAL4^rQ286.11, to induce ablation of glial cells, a spectrum of nervous system phenotypes are seen in embryonic hemisegments, which range from having a disrupted CNS and PNS pathways to being essentially normal. grim^Scer\UAS.cNa, Scer\GAL4^rQ286.11 embryos with highly aberrant nervous system patterning correlate with early evidence of glial ablation. From stage 13 onward, when the peripheral glia normally would have migrated into the periphery, the nuclei of the peripheral glial cells in these embryos remain outside the CNS. The peripheral nerves associated with the ablated glia are always defasciculated. In these embryos, sensory axons display a range of errors including stalls, improper fascicle choice, defasciculation, and misguidance on muscle. In glial ablated mutant embryos (driven by Scer\GAL4^rQ286.11 or Scer\GAL4^repo), sensory axons stall in their approach to the CNS. The pioneer motor axons exit the CNS along abnormal trajectories compared to the highly stereotypes pathways observed in wild-type. When grim^Scer\UAS.cNa is driven by Scer\GAL4^rQ14.7, mutant embryos do not show any stalling of sensory neurons. When grim^Scer\UAS.cNa is driven by Scer\GAL4^rQ286.11 or Scer\GAL4^repo, segments that show evidence of glial loss also show sensory stalls at 76% and 85% respectively. Axons cross between the anterior and posterior fascicles in about 50% of hemisegments, or cross the segment boundary at a similar frequency when grim^Scer\UAS.cNa is driven by either Scer\GAL4^rQ286.11 or Scer\GAL4^repo. In grim^Scer\UAS.cNa, Scer\GAL4^rQ286.11 embryos The lch neurites commonly stall at the transition zone and show pathfinding errors as they approach the CNS. Very often the axons head posteriorly and enter the CNS incorrectly toward the posterior fascicle route. The four lch axon projections also show significant defasciculation in some segments. Some sensory neurons migrate to a much lower focal plane in the ventral CNS region than do those in wild-type. In some embryos, lch axons are observed that project along the ventral muscles that lie just beneath the CNS. Also, in the absence of peripheral glia, lch neurons do not consistently migrate along VUM motor neuron tracts, which normally fasciculate with the lch neurons. (Sepp et al., 2001) When grim^Scer\UAS.cNa is driven by Scer\GAL4^Gp150-52A, embryos typically exhibit a loss of all midline glia most segments of the ventral nerve cord and also exhibit a fusion of several commissural axon bundles. (Wing et al., 1998)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement Reference Scer\GAL4^Gp150-52A, grim^Scer\UAS.cNa has increased cell death phenotype, enhanceable by Scer\GAL4^Gp150-52A/rpr^C.Scer\UAS (Wing et al., 1998)
Suppressed by
Statement Reference grim^Scer\UAS.cNa has increased cell death phenotype, suppressible by Scer\GAL4^Gp150-52A/BacA\p35^Scer\UAS.cHa (Wing et al., 1998) Scer\GAL4^Aug21, grim^Scer\UAS.cNa has lethal \| prepupal stage phenotype, suppressible by EcR^dsRNA.hs.PL, Scer\GAL4^Aug21 (Liu et al., 2009)
NOT suppressed by
Statement Reference Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, grim^Scer\UAS.cNa has lethal phenotype, non-suppressible by Iap2^Scer\UAS.cWa, Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF (Wing et al., 1998) Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, grim^Scer\UAS.cNa has lethal phenotype, non-suppressible by Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF/th^{Scer\UAS.T:Ivir\HA1} (Wing et al., 2001) Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, grim^Scer\UAS.cNa has lethal phenotype, non-suppressible by Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF/th^SL (Wing et al., 2001) Scer\GAL4^Gp150-52A, grim^Scer\UAS.cNa has increased cell death phenotype, non-suppressible by Iap2^Scer\UAS.cWa, Scer\GAL4^Gp150-52A (Wing et al., 1998)
Enhancer of
Statement Reference grim^Scer\UAS.cNa/Scer\GAL4^Gp150-52A is an enhancer of increased cell death phenotype of Scer\GAL4^Gp150-52A, rpr^C.Scer\UAS (Wing et al., 1998)
Suppressor of
Statement Reference grim^Scer\UAS.cNa/Scer\GAL4^vg.PM is a suppressor \| partially of lethal \| pupal stage phenotype of Scer\GAL4^vg.PM, stwl^UY823 (Brun et al., 2006)
Other
Statement Reference Scer\GAL4^Gp150-52A, grim^Scer\UAS.cNa, morgue^EP2367 has increased cell death phenotype (Wing et al., 2002, Wing et al., 2002)
Phenotype Manifest In
Enhanced by
Statement Reference Scer\GAL4^Gp150-52A, grim^Scer\UAS.cNa has midline glial cell phenotype, enhanceable by Scer\GAL4^Gp150-52A/morgue^EP2367 (Wing et al., 2002) Scer\GAL4^Gp150-52A, grim^Scer\UAS.cNa has midline glial cell phenotype, enhanceable by Scer\GAL4^Gp150-52A/rpr^C.Scer\UAS (Wing et al., 1998) Scer\GAL4^Gp150-52A, grim^Scer\UAS.cNa has midline glial cell phenotype, enhanceable by Scer\GAL4^Gp150-52A/rpr^Scer\UAS.cZa (Wing et al., 1998) Scer\GAL4^Gp150-52A, grim^Scer\UAS.cNa has midline glial cell phenotype, enhanceable by W^Scer\UAS.cZa/Scer\GAL4^Gp150-52A (Wing et al., 1998)
Suppressed by
Statement Reference grim^Scer\UAS.cNa has midline glial cell phenotype, suppressible by Scer\GAL4^Gp150-52A/BacA\p35^Scer\UAS.cHa (Wing et al., 1998) Scer\GAL4^Gp150-52A, grim^Scer\UAS.cNa has ventral midline phenotype, suppressible by Scer\GAL4^Gp150-52A/th^{Scer\UAS.T:Ivir\HA1} (Wing et al., 2001) Scer\GAL4^He.PZ, grim^Scer\UAS.cNa has embryonic/larval hemolymph \| third instar larval stage phenotype, suppressible by Spn27A^Scer\UAS.cLa/Scer\GAL4^He.PZ (Bidla et al., 2007)
NOT suppressed by
Statement Reference Scer\GAL4^Gp150-52A, grim^Scer\UAS.cNa has midline glial cell phenotype, non-suppressible by Iap2^Scer\UAS.cWa, Scer\GAL4^Gp150-52A (Wing et al., 1998)
Enhancer of
Statement Reference grim^Scer\UAS.cNa/Scer\GAL4^Gp150-52A is an enhancer of midline glial cell phenotype of Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, rpr^Scer\UAS.cZa (Wing et al., 1998) grim^Scer\UAS.cNa/Scer\GAL4^Gp150-52A is an enhancer of midline glial cell phenotype of Scer\GAL4^Gp150-52A, rpr^C.Scer\UAS (Wing et al., 1998) grim^Scer\UAS.cNa/Scer\GAL4^Gp150-52A is an enhancer of midline glial cell phenotype of Scer\GAL4^Gp150-52A, W^Scer\UAS.cZa (Wing et al., 1998)
Other
Statement Reference Scer\GAL4^Gp150-52A, grim^Scer\UAS.cNa, morgue^EP2367 has presumptive embryonic/larval central nervous system phenotype (Wing et al., 2002, Wing et al., 2002)
Additional Comments
Genetic Interactions
Statement Reference When reared without heat-shock induction, about 10% of animals expressing Scer\GAL4[Aug21]-driven grim[Scer\UAS.cNa] in the presence of EcR[dsRNA.hs.PL] survive to pharate adult stage and less than half of those emerge as adults. (Liu et al., 2009) Expression of Spn27A[Scer\UAS.cLa] in larval hemocytes expressing grim[Scer\UAS.cNa] under the control of Scer\GAL4[He.PZ] results in almost no melanization. (Bidla et al., 2007) Co-expression of morgue^EP2367 and grim^Scer\UAS.cNa under the control of Scer\GAL4^Gp150-52A in embryos in the central nervous system midline results in more severe loss of midline glia than seen in embryos expressing grim^Scer\UAS.cNa alone under the control of Scer\GAL4^Gp150-52A. (Wing et al., 2002) The addition of th^{Scer\UAS.T:Ivir\HA1} completely suppresses the ventral midline phenotype seen in rpr^Scer\UAS.cZa, Scer\GAL4^Gp150-52A flies alone. (Wing et al., 2001) When grim^Scer\UAS.cNa and rpr^Scer\UAS.cZa are coexpressed, all the midline glia and some VUM neurons are eliminated. When grim^Scer\UAS.cNa and W^Scer\UAS.cZa are coexpressed, all the midline glia and some VUM neurons are eliminated. co-expression of rpr^C.Scer\UAS and grim^Scer\UAS.cNa leads to a loss of both midline glia and VUM neurons from all segments of the nerve cord. Expression of Iap2^Scer\UAS.cWa fails to rescue the lethality phenotype seen in grim^Scer\UAS.cNa, Scer\GAL4^GMR.PF flies; less than 1% of animals survive and those exhibit a loss of ommatidia. (Wing et al., 1998)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Comments
Stocks ( 0 )

Notes on Origin
Discoverer	J.R. Nambu

External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 3 )
Reported As
Symbol Synonym	grim^Scer\UAS.cNa grim^UAS.cNa
Name Synonym	Saccharomyces cerevisiae UAS construct a of Nambu (Chen et al., 1998)
Secondary FlyBase IDs

References ( 21 )

Generate a list of	All references relating to this allele ( 21 )

List References by type	Research paper ( 21 )
Recent research papers ( 3 )
	Parvy et al., 2012, PLoS Genet. 8(8): e1002925 Drosophila melanogaster Acetyl-CoA-Carboxylase Sustains a Fatty Acid-Dependent Remote Signal to Waterproof the Respiratory System. [FBrf0219401] Abdou et al., 2011, Insect Biochem. Mol. Biol. 41(12): 938--945 Drosophila Met and Gce are partially redundant in transducing juvenile hormone action. [FBrf0216586] Ou et al., 2011, PLoS Biol. 9(9): e1001160 Nuclear Receptor DHR4 Controls the Timing of Steroid Hormone Pulses During Drosophila Development. [FBrf0216318] Show all research papers ...

Allele Dmel\grimScer\UAS.cNa

Allele Dmel\grim^Scer\UAS.cNa