scholarly journals Drosophila Tufted Is a Gain-of-Function Allele of the Proneural Gene amos

Genetics ◽  
2003 ◽  
Vol 163 (4) ◽  
pp. 1413-1425 ◽  
Author(s):  
Eric C Lai
Keyword(s):  
Molecular Evidence ◽  
Proneural Gene ◽  
Sensory Organs ◽  
Gain Of Function ◽  
Proneural Genes ◽  
Bhlh Proteins ◽  
Do So ◽  
Drosophila Mutant

Abstract Tufted is a classical Drosophila mutant characterized by a large number of ectopic mechanosensory bristles on the dorsal mesothorax. Unlike other ectopic bristle mutants, Tufted is epistatic to achaete and scute, the proneural genes that normally control the development of these sensory organs. In this report, I present genetic and molecular evidence that Tufted is a gain-of-function allele of the proneural gene amos that ectopically activates mechanosensory neurogenesis. I also systematically examine the ability of the various proneural bHLH proteins to cross-activate each other and find that their ability to do so is in general relatively limited, despite their common ability to induce the formation of mechanosensory bristles. This phenomenon seems instead to be related to their shared ability to activate Asense and Senseless.

scholarly journals A Gain-of-Function Screen for Genes That Affect the Development of the Drosophila Adult External Sensory Organ

Genetics ◽  
2000 ◽  
Vol 155 (2) ◽  
pp. 733-752 ◽  
Author(s):  
Salim Abdelilah-Seyfried ◽  
Yee-Ming Chan ◽  
Chaoyang Zeng ◽  
Nicholas J Justice ◽  
Susan Younger-Shepherd ◽  
...  
Keyword(s):  
Nervous System ◽  
Peripheral Nervous System ◽  
Cell Fate ◽  
P Element ◽  
External Support ◽  
Sensory Organ ◽  
Sensory Organs ◽  
Gain Of Function ◽  
Asymmetric Cell Divisions ◽  
Single Precursor

Abstract The Drosophila adult external sensory organ, comprising a neuron and its support cells, is derived from a single precursor cell via several asymmetric cell divisions. To identify molecules involved in sensory organ development, we conducted a tissue-specific gain-of-function screen. We screened 2293 independent P-element lines established by P. Rørth and identified 105 lines, carrying insertions at 78 distinct loci, that produced misexpression phenotypes with changes in number, fate, or morphology of cells of the adult external sensory organ. On the basis of the gain-of-function phenotypes of both internal and external support cells, we subdivided the candidate lines into three classes. The first class (52 lines, 40 loci) exhibits partial or complete loss of adult external sensory organs. The second class (38 lines, 28 loci) is associated with increased numbers of entire adult external sensory organs or subsets of sensory organ cells. The third class (15 lines, 10 loci) results in potential cell fate transformations. Genetic and molecular characterization of these candidate lines reveals that some loci identified in this screen correspond to genes known to function in the formation of the peripheral nervous system, such as big brain, extra macrochaetae, and numb. Also emerging from the screen are a large group of previously uncharacterized genes and several known genes that have not yet been implicated in the development of the peripheral nervous system.

Neurogenic expression of snail is controlled by separable CNS and PNS promoter elements

Development ◽  
1994 ◽  
Vol 120 (1) ◽  
pp. 199-207 ◽  
Author(s):  
Y.T. Ip ◽  
M. Levine ◽  
E. Bier
Keyword(s):  
Regulatory Region ◽  
Neural Element ◽  
Proneural Gene ◽  
Lacz Expression ◽  
Proneural Genes ◽  
Growing Body ◽  
Mesoderm Formation ◽  
Separate Control ◽  
Early Neurogenesis ◽  
Developing Nervous System

The Drosophila snail (sna) gene is first expressed in cells giving rise to mesoderm and is required for mesoderm formation. sna is subsequently expressed in the developing nervous system. sna expression during neurogenesis evolves from segmentally repeated neuroectodermal domains to a pan-neural pattern. We have identified a 2.8 kb regulatory region of the sna promoter that drives LacZ expression in a faithful neuronal pattern. Deletion analysis of this region indicates that the pan-neural element is composed of separable CNS and PNS components. This finding is unexpected since all known genes controlling early neurogenesis, including the proneural genes (i.e. da and AS-C), are expressed in both the CNS and PNS. We also show that expression of sna during neurogenesis is largely independent of the proneural genes da and AS-C. The separate control of CNS and PNS sna expression and independence of proneural gene regulation add to a growing body of evidence that current genetic models of neurogenesis are substantially incomplete.

asense is a Drosophila neural precursor gene and is capable of initiating sense organ formation

Development ◽  
1993 ◽  
Vol 119 (1) ◽  
pp. 1-17 ◽  
Author(s):  
M. Brand ◽  
A.P. Jarman ◽  
L.Y. Jan ◽  
Y.N. Jan
Keyword(s):  
Ectopic Expression ◽  
Sense Organ ◽  
Neural Precursor Cells ◽  
Neural Precursor ◽  
Gene Products ◽  
Proneural Gene ◽  
Proneural Genes ◽  
Helix Loop Helix ◽  
Normal Gene ◽  
Proneural Cluster

Neural precursor cells in Drosophila arise from the ectoderm in the embryo and from imaginal disc epithelia in the larva. In both cases, this process requires daughterless and the proneural genes achaete, scute and lethal-of-scute of the achaete-scute complex. These genes encode basic helix-loop-helix proteins, which are nuclear transcription factors, as does the asense gene of the achaete-scute complex. Our studies suggest that asense is a neural precursor gene, rather than a proneural gene. Unlike the proneural achaete-scute gene products, the asense RNA and protein are found in the neural precursor during its formation, but not in the proneural cluster of cells that gives rise to the neural precursor cell. Also, asense expression persists longer during neural precursor development than the proneural gene products; it is still expressed after the first division of the neural precursor. Moreover, asense is likely to be downstream of the proneural genes, because (1) asense expression is affected in proneural and neurogenic mutant backgrounds, (2) ectopic expression of asense protein with an intact DNA-binding domain bypasses the requirement for achaete and scute in the formation of imaginal sense organs. We further note that asense ectopic expression is capable of initiating the sense organ fate in cells that do not normally require the action of asense. Our studies therefore serve as a cautionary note for the inference of normal gene function based on the gain-of-function phenotype after ectopic expression.

Neurogenic genes control gene expression at the transcriptional level in early neurogenesis and in mesectoderm specification

Development ◽  
1995 ◽  
Vol 121 (1) ◽  
pp. 219-224 ◽  
Author(s):  
M.D. Martin-Bermudo ◽  
A. Carmena ◽  
F. Jimenez
Keyword(s):  
Posttranscriptional Regulation ◽  
Drosophila Embryo ◽  
Transcriptional Level ◽  
Proneural Gene ◽  
Proneural Genes ◽  
Protein Levels ◽  
Neurogenic Genes ◽  
The Central Nervous System ◽  
Early Neurogenesis ◽  
The Relationship

The development of the central nervous system in the Drosophila embryo is initiated by the acquisition of neural potential by clusters of ectodermal cells, promoted by the activity of proneural genes. Proneural gene function is antagonized by neurogenic genes, resulting in the realization of the neural potential in a single cell per cluster. To analyse the relationship between proneural and neurogenic genes, we have studied, in specific proneural clusters and neuroblasts of wild-type and neurogenic mutants embryos, the expression at the RNA and protein levels of lethal of scute, the most important known proneural gene in central neurogenesis. We find that the restriction of lethal of scute expression that accompanies the restriction of the neural potential to the delaminating neuroblast is regulated at the transcriptional level by neurogenic genes. These genes, however, do not control the size of proneural clusters. Moreover, available antibodies do not provide evidence for an hypothetical posttranscriptional regulation of proneural proteins by neurogenic genes. We also find that neurogenic genes are required for the specification of the mesectoderm. This has been shown for neuralized and Notch, and could also be the case for Delta and for the Enhancer of split gene complex. Neurogenic genes would control at the transcriptional level the repression of proneural genes and the activation of single-minded in the anlage of the mesectoderm.

scholarly journals Use of cranial characters in taxonomy of the Minnesota wolf (Canis sp.)

2011 ◽  
Vol 89 (12) ◽  
pp. 1188-1194 ◽  
Author(s):  
L. David Mech ◽  
Ronald M. Nowak ◽  
Sanford Weisberg
Keyword(s):  
Endangered Species ◽  
Canis Lupus ◽  
Molecular Evidence ◽  
Skull Morphology ◽  
Species List ◽  
Eastern Wolf ◽  
Skull Measurements ◽  
Recent Government ◽  
Do So

Minnesota wolves (Canis sp.) sometimes are reported to have affinity to a small, narrow-skulled eastern form ( Canis lupus lycaon Schreber, 1775) and sometimes to a larger, broader western form ( Canis lupus nubilus Say, 1823). We found that pre-1950 Minnesota wolf skulls were similar in size to those of wolves from southeastern Ontario and smaller than those of western wolves. However, Minnesota wolf skulls during 1970–1976 showed a shift to the larger, western form. Although Minnesota skull measurements after 1976 were unavailable, rostral ratios from 1969 through 1999 were consistent with hybridization between the smaller eastern wolf and the western form. Our findings help resolve the different taxonomic interpretations of Minnesota skull morphology and are consistent with molecular evidence of recent hybridization or intergradation of the two forms of wolves in Minnesota. Together these data indicate that eastern- and western-type wolves historically mixed and hybridized in Minnesota and continue to do so. Our findings are relevant to a recent government proposal to delist wolves from the endangered species list in Minnesota and surrounding states.

scholarly journals Rough eyeIs a Gain-of-Function Allele ofamosThat Disrupts Regulation of the Proneural GeneatonalDuring Drosophila Retinal Differentiation

Genetics ◽  
2002 ◽  
Vol 160 (2) ◽  
pp. 623-635 ◽  
Author(s):  
Françoise Chanut ◽  
Katherine Woo ◽  
Shalini Pereira ◽  
Terrence J Donohoe ◽  
Shang-Yu Chang ◽  
...  
Keyword(s):  
Molecular Characterization ◽  
Chromosomal Inversion ◽  
Developmental Defect ◽  
Proneural Gene ◽  
Bhlh Gene ◽  
Residual Function ◽  
Dominant Mutation ◽  
Gain Of Function ◽  
Irregular Distribution

AbstractThe regular organization of the ommatidial lattice in the Drosophila eye originates in the precise regulation of the proneural gene atonal (ato), which is responsible for the specification of the ommatidial founder cells R8. Here we show that Rough eye (Roi), a dominant mutation manifested by severe roughening of the adult eye surface, causes defects in ommatidial assembly and ommatidial spacing. The ommatidial spacing defect can be ascribed to the irregular distribution of R8 cells caused by a disruption of the patterning of ato expression. Disruptions in the recruitment of other photoreceptors and excess Hedgehog production in differentiating cells may further contribute to the defects in ommatidial assembly. Our molecular characterization of the Roi locus demonstrates that it is a gain-of-function mutation of the bHLH gene amos that results from a chromosomal inversion. We show that Roi can rescue the retinal developmental defect of ato1 mutants and speculate that amos substitutes for some of ato's function in the eye or activates a residual function of the ato1 allele.

scholarly journals Neurog2 and Ascl1 together regulate a postmitotic derepression circuit to govern laminar fate specification in the murine neocortex

2017 ◽  
Vol 114 (25) ◽  
pp. E4934-E4943 ◽  
Author(s):  
Daniel J. Dennis ◽  
Grey Wilkinson ◽  
Saiqun Li ◽  
Rajiv Dixit ◽  
Lata Adnani ◽  
...  
Keyword(s):  
Cell Fate ◽  
Deep Layer ◽  
Projection Neurons ◽  
Cell Fate Specification ◽  
Transcriptional Repressors ◽  
Gain Of Function ◽  
Proneural Genes ◽  
Fate Specification ◽  
Layer V ◽  
Layer Vi

A derepression mode of cell-fate specification involving the transcriptional repressors Tbr1, Fezf2, Satb2, and Ctip2 operates in neocortical projection neurons to specify six layer identities in sequence. Less well understood is how laminar fate transitions are regulated in cortical progenitors. The proneural genes Neurog2 and Ascl1 cooperate in progenitors to control the temporal switch from neurogenesis to gliogenesis. Here we asked whether these proneural genes also regulate laminar fate transitions. Several defects were observed in the derepression circuit in Neurog2−/−;Ascl1−/− mutants: an inability to repress expression of Tbr1 (a deep layer VI marker) during upper-layer neurogenesis, a loss of Fezf2+/Ctip2+ layer V neurons, and precocious differentiation of normally late-born, Satb2+ layer II–IV neurons. Conversely, in stable gain-of-function transgenics, Neurog2 promoted differentiative divisions and extended the period of Tbr1+/Ctip2+ deep-layer neurogenesis while reducing Satb2+ upper-layer neurogenesis. Similarly, acute misexpression of Neurog2 in early cortical progenitors promoted Tbr1 expression, whereas both Neurog2 and Ascl1 induced Ctip2. However, Neurog2 was unable to influence the derepression circuit when misexpressed in late cortical progenitors, and Ascl1 repressed only Satb2. Nevertheless, neurons derived from late misexpression of Neurog2 and, to a lesser extent, Ascl1, extended aberrant subcortical axon projections characteristic of early-born neurons. Finally, Neurog2 and Ascl1 altered the expression of Ikaros and Foxg1, known temporal regulators. Proneural genes thus act in a context-dependent fashion as early determinants, promoting deep-layer neurogenesis in early cortical progenitors via input into the derepression circuit while also influencing other temporal regulators.

The ventral nervous system defective gene controls proneural gene expression at two distinct steps during neuroblast formation in Drosophila

Development ◽  
1994 ◽  
Vol 120 (6) ◽  
pp. 1517-1524 ◽  
Author(s):  
J.B. Skeath ◽  
G.F. Panganiban ◽  
S.B. Carroll
Keyword(s):  
Gene Expression ◽  
Nervous System ◽  
Cluster Formation ◽  
Regulatory Region ◽  
Regulatory Elements ◽  
Drosophila Embryo ◽  
Proneural Gene ◽  
Lacz Reporter ◽  
Proneural Genes ◽  
Proneural Cluster

Within the Drosophila embryo, the formation of many neuroblasts depends on the functions of the proneural genes of the achaete-scute complex (AS-C): achaete (ac), scute (sc) and lethal of scute (l'sc), and the gene ventral nervous system defective (vnd). Here, we show that vnd controls neuroblast formation, in part, through its regulation of the proneural genes of the AS-C. vnd is absolutely required to activate ac, sc and l'sc gene expression in proneural clusters in specific domains along the medial column of the earliest arising neuroblasts. Using ac-lacZ reporter constructs, we determined that vnd controls proneural gene expression at two distinct steps during neuroblast formation through separable regulatory regions. First, vnd is required to activate proneural cluster formation within the medial column of every other neuroblast row through regulatory elements located 3′ to ac; second, through a 5′ regulatory region, vnd functions to increase or maintain proneural gene expression in the cell within the proneural cluster that normally becomes the neuroblast. By following neuroblast segregation in vnd mutant embryos, we show that the neuroectoderm forms normally and that the defects in neuroblast formation are specific to particular proneural clusters.

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