eagle is required for the specification of serotonin neurons and other neuroblast 7–3 progeny in the Drosophila CNS

Development ◽  
1998 ◽  
Vol 125 (3) ◽  
pp. 463-472 ◽  
Author(s):  
M.J. Lundell ◽  
J. Hirsh
Keyword(s):  
Molecular Markers ◽  
Zinc Finger ◽  
Nerve Cord ◽  
Dramatic Reduction ◽  
Loss Of Function ◽  
Animal Kingdom ◽  
Zinc Finger Gene ◽  
Serotonin Neurons ◽  
Hypomorphic Alleles ◽  
Serotonin Cells

During development of the Drosophila nerve cord, neuroblast 7–3 gives rise to a pair of mitotic sister serotonin neurons in each hemisegment. Here we show that the zinc finger gene eagle, which is expressed in neuroblast 7–3, is essential for specifying the fate of serotonin neurons. We find that loss-of-function eagle mutations produce an unusual differential phenotype with respect to the sister serotonin cells and that eagle is necessary for the maintenance of engrailed and zfh-2 expression in the serotonin neurons. We present a model that uniquely identifies all progeny neurons in the neuroblast 7–3 lineage based on the expression of specific molecular markers, position within the nerve cord and the effect of eagle loss-of-function mutations. Although serotonin is an important neurotransmitter conserved throughout the animal kingdom, we show that hypomorphic alleles of eagle can produce viable adults that have a dramatic reduction in the number of serotonin-producing neurons.

Transcriptional regulation of the Hedgehog effector CI by the zinc-finger gene combgap

Development ◽  
2000 ◽  
Vol 127 (19) ◽  
pp. 4095-4103 ◽  
Author(s):  
G.L. Campbell ◽  
A. Tomlinson
Keyword(s):  
Transcription Factors ◽  
Cell Fate ◽  
Zinc Finger ◽  
Transcriptional Activation ◽  
Dna Binding Protein ◽  
Loss Of Function ◽  
Cubitus Interruptus ◽  
Anterior Compartment ◽  
Zinc Finger Gene ◽  
Animal Development

Members of the Hedgehog (HH) family of secreted signaling molecules specify cell fate during animal development by controlling the activity of members of the Gli family of zinc-finger transcription factors in responding cells. In Drosophila the Gli homolog, cubitus interruptus (CI), is expressed only in the anterior compartment where it represses targets such as the signaling molecule genes decapentaplegic (dpp) and wingless (wg). HH is expressed in the posterior and diffuses into the anterior where it antagonizes CI repression resulting in dpp and wg expression immediately anterior to the compartment border. Reducing CI levels results in misexpression of wg and dpp, while CI misexpression in the posterior disrupts differentiation. Thus, normal disc patterning requires high levels of CI in the anterior and the absence of CI in the posterior. Here we show that mutations in combgap (cg) result in deregulation of CI expression, which is now expressed at much lower levels and ubiquitously, i.e., also in the posterior. Consequently, cg mutants phenocopy ci loss-of-function mutants in the anterior and ci gain-of-function mutants in the posterior. cg encodes a putative DNA-binding protein that regulates both transcriptional activation and repression of the ci gene.

scholarly journals Mini-Review Regarding the Applicability of Genome Editing Techniques Developed for Studying Infertility

Diagnostics ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 246
Author(s):  
Bogdan Doroftei ◽  
Ovidiu-Dumitru Ilie ◽  
Maria Puiu ◽  
Alin Ciobica ◽  
Ciprian Ilea
Keyword(s):  
Motor Activity ◽  
Experimental Model ◽  
Zinc Finger ◽  
Biomedical Research ◽  
Zinc Finger Nucleases ◽  
Loss Of Function ◽  
Transcription Activator ◽  
Phenotypic Changes ◽  
Wide Range ◽  
Short Palindromic Repeat

Infertility is a highly debated topic today. It has been long hypothesized that infertility has an idiopathic cause, but recent studies demonstrated the existence of a genetic substrate. Fortunately, the methods of editing the human genome proven to be revolutionary. Following research conducted, we identified a total of 21 relevant studies; 14 were performed on mice, 5 on zebrafish and 2 on rats. We concluded that over forty-four genes in total are dispensable for fertility in both sexes without affecting host homeostasis. However, there are genes whose loss-of-function induces moderate to severe phenotypic changes in both sexes. There were situations in which the authors reported infertility, exhibited by the experimental model, or other pathologies such as cryptorchidism, cataracts, or reduced motor activity. Overall, zinc-finger nucleases (ZFNs), transcription activator-like effector nucleases (TALENs), and clustered regularly interspaced short palindromic repeat (CRISPR)/Cas9 are techniques that offer a wide range of possibilities for studying infertility, even to create mutant variants. It can be concluded that ZFNs, TALENs, and CRISPR/Cas9 are crucial tools in biomedical research.

scholarly journals Trans-acting Factors Required for Inclusion of Regulated Exons in the Ultrabithorax mRNAs of Drosophila melanogaster

Genetics ◽  
1999 ◽  
Vol 151 (4) ◽  
pp. 1517-1529 ◽  
Author(s):  
James M Burnette ◽  
Allyson R Hatton ◽  
A Javier Lopez
Keyword(s):  
Drosophila Melanogaster ◽  
Alternative Splicing ◽  
P Element ◽  
Splicing Factors ◽  
Loss Of Function ◽  
Large Collection ◽  
Splicing Pattern ◽  
Alternatively Spliced ◽  
Hypomorphic Alleles

Abstract Alternatively spliced Ultrabithorax mRNAs differ by the presence of internal exons mI and mII. Two approaches were used to identify trans-acting factors required for inclusion of these cassette exons. First, mutations in a set of genes implicated in the control of other alternative splicing decisions were tested for dominant effects on the Ubx alternative splicing pattern. To identify additional genes involved in regulation of Ubx splicing, a large collection of deficiencies was tested first for dominant enhancement of the haploinsufficient Ubx haltere phenotype and second for effects on the splicing pattern. Inclusion of the cassette exons in Ubx mRNAs was reduced strongly in heterozygotes for hypomorphic alleles of hrp48, which encodes a member of the hnRNP A/B family and is implicated in control of P-element splicing. Significant reductions of mI and mII inclusion were also observed in heterozygotes for loss-of-function alleles of virilizer, fl(2)d, and crooked neck. The products of virilizer and fl(2)d are also required for Sxl autoregulation at the level of splicing; crooked neck encodes a protein with structural similarities to yeast-splicing factors Prp39p and Prp42p. Deletion of at least five other loci caused significant reductions in the inclusion of mI and/or mII. Possible roles of identified factors are discussed in the context of the resplicing strategy for generation of alternative Ubx mRNAs.

scholarly journals Parkin interacting substrate zinc finger protein 746 is a pathological mediator in Parkinson’s disease

Brain ◽  
2019 ◽  
Vol 142 (8) ◽  
pp. 2380-2401 ◽  
Author(s):  
Saurav Brahmachari ◽  
Saebom Lee ◽  
Sangjune Kim ◽  
Changqing Yuan ◽  
Senthilkumar S Karuppagounder ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Critical Role ◽  
Trna Synthetase ◽  
Loss Of Function ◽  
Substrate Protein ◽  
Finger Protein ◽  
Sporadic Parkinson’S Disease

Abstract α-Synuclein misfolding and aggregation plays a major role in the pathogenesis of Parkinson’s disease. Although loss of function mutations in the ubiquitin ligase, parkin, cause autosomal recessive Parkinson’s disease, there is evidence that parkin is inactivated in sporadic Parkinson’s disease. Whether parkin inactivation is a driver of neurodegeneration in sporadic Parkinson’s disease or a mere spectator is unknown. Here we show that parkin in inactivated through c-Abelson kinase phosphorylation of parkin in three α-synuclein-induced models of neurodegeneration. This results in the accumulation of parkin interacting substrate protein (zinc finger protein 746) and aminoacyl tRNA synthetase complex interacting multifunctional protein 2 with increased parkin interacting substrate protein levels playing a critical role in α-synuclein-induced neurodegeneration, since knockout of parkin interacting substrate protein attenuates the degenerative process. Thus, accumulation of parkin interacting substrate protein links parkin inactivation and α-synuclein in a common pathogenic neurodegenerative pathway relevant to both sporadic and familial forms Parkinson’s disease. Thus, suppression of parkin interacting substrate protein could be a potential therapeutic strategy to halt the progression of Parkinson’s disease and related α-synucleinopathies.

Identification and characterization of a zinc finger gene (ZNF213) from 16p13.3

1999 ◽  
Vol 1444 (2) ◽  
pp. 218-230 ◽  
Author(s):  
Xiaoguang Chen ◽  
Melanie Hamon ◽  
Zuoming Deng ◽  
Michael Centola ◽  
Raman Sood ◽  
...  
Keyword(s):  
Zinc Finger ◽  
Zinc Finger Gene ◽  
Identification And Characterization

Comprehensive analysis of CCCH-type zinc finger gene family in citrus (Clementine mandarin) by genome-wide characterization

2014 ◽  
Vol 289 (5) ◽  
pp. 855-872 ◽  
Author(s):  
Shengrui Liu ◽  
Muhammad Rehman Gul Khan ◽  
Yongping Li ◽  
Jinzhi Zhang ◽  
Chungen Hu
Keyword(s):  
Gene Family ◽  
Zinc Finger ◽  
Comprehensive Analysis ◽  
Zinc Finger Gene ◽  
Genome Wide

scholarly journals Expression of the zinc finger gene EVI-1 in ovarian and other cancers

1996 ◽  
Vol 74 (10) ◽  
pp. 1518-1525 ◽  
Author(s):  
DJ Brooks ◽  
S Woodward ◽  
FH Thompson ◽  
B Dos Santos ◽  
M Russell ◽  
...  
Keyword(s):  
Zinc Finger ◽  
Zinc Finger Gene

scholarly journals Molecular study of the hematopoietic zinc finger gene in three unrelated families with gray platelet syndrome

2005 ◽  
Vol 3 (9) ◽  
pp. 2077-2080 ◽  
Author(s):  
L. BÉNIT ◽  
E. M. CRAMER ◽  
J. M. MASSÉ ◽  
I. DUSANTER-FOURT ◽  
R. FAVIER
Keyword(s):  
Zinc Finger ◽  
Molecular Study ◽  
Zinc Finger Gene ◽  
Gray Platelet Syndrome

Isolation and expression of linked zinc finger gene clusters on human chromosome 11q

Genomics ◽  
1992 ◽  
Vol 14 (4) ◽  
pp. 970-978 ◽  
Author(s):  
Mary Saleh ◽  
Licia Selleri ◽  
Peter F.R. Little ◽  
Glen A. Evans
Keyword(s):  
Human Chromosome ◽  
Zinc Finger ◽  
Gene Clusters ◽  
Zinc Finger Gene
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