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.

Distribution and function of the lethal of scute gene product during early neurogenesis in Drosophila

Development ◽  
1991 ◽  
Vol 113 (2) ◽  
pp. 445-454 ◽  
Author(s):  
M.D. Martin-Bermudo ◽  
C. Martinez ◽  
A. Rodriguez ◽  
F. Jimenez
Keyword(s):  
Central Nervous System ◽  
Drosophila Embryo ◽  
Fushi Tarazu ◽  
Phenotypic Analysis ◽  
Neuronal Identity ◽  
The Central Nervous System ◽  
Early Neurogenesis ◽  
And Function ◽  
High Degree ◽  
Peripheral Sensory

Genes of the achaete-scute complex (ASC) participate in the formation of the central nervous system in the Drosophila embryo. Previous genetic analyses have indicated that lethal of scute (l'sc) is the most important gene of the complex in that process. We have obtained antibodies against the l'sc protein to study the expression of the gene during early neurogenesis. The protein is found in groups of embryonic neuroectodermal cells, analogous to the proneural clusters that precede the appearance of precursors of peripheral sensory organs in imaginal epithelia. The groups appear in different regions of the neuroectoderm, accompanying the three successive waves of neuroblast segregation. Most neuroblasts delaminate from these clusters and express position-specific levels of l'sc protein. No significant differences have been found between the distribution of l'sc RNA and protein. Phenotypic analysis of a l'sc deficiency has shown that the gene is required for neuroblast commitment, although this requirement is less widespread than the domain of l'sc expression, suggesting a high degree of redundancy in the function of genes that participate in the process of neuroblast segregation. The ASC genes have been postulated to play a role in the control of NB identity, revealed by the generation of a defined lineage of identifiable neurons. However, our study in l'sc mutants of the expression of fushi tarazu, engrailed, and even-skipped, used as markers of neuronal identity, has not provided evidence to support this hypothesis.

Regulation of proneural gene expression and cell fate during neuroblast segregation in the Drosophila embryo

Development ◽  
1992 ◽  
Vol 114 (4) ◽  
pp. 939-946 ◽  
Author(s):  
J.B. Skeath ◽  
S.B. Carroll
Keyword(s):  
Gene Expression ◽  
Cell Fate ◽  
Single Cells ◽  
Regulatory Protein ◽  
Drosophila Embryo ◽  
Proneural Gene ◽  
Developmental Pathway ◽  
Neurogenic Genes ◽  
Temporal And Spatial ◽  
Epidermal Development

The Drosophila embryonic central nervous system develops from sets of progenitor neuroblasts which segregate from the neuroectoderm during early embryogenesis. Cells within this region can follow either the neural or epidermal developmental pathway, a decision guided by two opposing classes of genes. The proneural genes, including the members of the achaete-scute complex (AS-C), promote neurogenesis, while the neurogenic genes prevent neurogenesis and facilitate epidermal development. To understand the role that proneural gene expression and regulation play in the choice between neurogenesis and epidermogenesis, we examined the temporal and spatial expression pattern of the achaete (ac) regulatory protein in normal and neurogenic mutant embryos. The ac protein is first expressed in a repeating pattern of four ectodermal cell clusters per hemisegment. Even though 5–7 cells initially express ac in each cluster, only one, the neuroblast, continues to express ac. The repression of ac in the remaining cells of the cluster requires zygotic neurogenic gene function. In embryos lacking any one of five genes, the restriction of ac expression to single cells does not occur; instead, all cells of each cluster continue to express ac, enlarge, delaminate and become neuroblasts. It appears that one key function of the neurogenic genes is to silence proneural gene expression within the nonsegregating cells of the initial ectodermal clusters, thereby permitting epidermal development.

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.

scholarly journals Long Non-coding RNA LINC01119 Promotes Neuropathic Pain by Stabilizing BDNF Transcript

2021 ◽  
Vol 14 ◽  
Author(s):  
Le Zhang ◽  
Hao Feng ◽  
Yanwu Jin ◽  
Yufeng Zhan ◽  
Qi Han ◽  
...  
Keyword(s):  
Nervous System ◽  
Neuropathic Pain ◽  
Rna Binding ◽  
Regulatory Mechanism ◽  
Rna Stability ◽  
Expression Level ◽  
Transcriptional Level ◽  
Bdnf Mrna ◽  
Protein Levels ◽  
The Central Nervous System

Neuropathic pain (NP) is caused by primary injury or dysfunction of the peripheral and the central nervous system. Long non-coding RNAs were critical regulators involved in nervous system diseases, however, the precise regulatory mechanism remains unclear. This study aims to uncover the essential role of LINC01119 in NP progression and further clarify the underlying regulatory mechanism at post-transcriptional level. LINC01119 was significantly upregulated in rats of spare nerve injury (SNI) group compared to sham group. Functionally, silencing of LINC01119 significantly alleviated the neuropathic pain-induced hypersensitivity and reduced the increase in IL−6, IL−1β, and TNF−α caused by SNI. Mechanistically, Brain-derived neurotrophic factor (BDNF) was identified as the functional target of LINC01119. Besides, an RNA binding protein, ELAVL1 could directly interact with LINC01119, and this formed LINC01119- ELAVL1 complex binds to BDNF mRNA, strengthening its RNA stability and increasing the expression level of BDNF at both transcript and protein levels. Clinically, serum LINC01119 was verified as a promising diagnostic biomarker for NP patients. LINC01119 induces NP progression via binding with ELAVL1 and increasing BDNF mRNA stability and expression level. Therefore, LINC01119 may serve as a promising diagnostic marker and therapeutic target for NP treatment.

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.

Evaluación Cognitiva Montreal y consumo de alcohol: Un diagnóstico descriptivo del deterioro cognitivo en estudiantes universitarios de Durango, México

2019 ◽  
pp. 28-38
Author(s):  
Karla Liliana Pérez-Sosa ◽  
Edgar Felipe Lares-Bayona
Keyword(s):  
Cognitive Impairment ◽  
Alcohol Consumption ◽  
Cognitive Functions ◽  
Toxic Substance ◽  
Female Gender ◽  
Diagnostic Tools ◽  
Cross Sectional ◽  
Probabilistic Study ◽  
The Central Nervous System ◽  
The Relationship

Alcohol is a toxic substance associated with acute and chronic disorders affecting the Central Nervous System and significantly altering brain function. Objective: To determine the relationship between cognitive impairment and alcohol consumption in university students of the Juárez University of the State of Durango. Methodology: It is a cross-sectional, descriptive, comparative, non-probabilistic study, for convenience. A database was designed on the results obtained in a clinical interview on alcohol consumption and the application of the Montreal Cognitive Assessment (MoCA) test. Contribution: The evaluation of cognitive functions show similar results, the male sex presented a better score in Attention and the female one in Orientation. More involvement was identified in the Deferred Memory functions in both groups. In relation to alcohol consumption, the cognitive functions evaluated show lower levels. The female gender was more evident cognitive impairment in relation to alcohol consumption being statistically significant (p <0.025). Alcohol consumption is a risky behavior that deserves to be recognized by the main actors about neurocognitive effects. Alcohol consumption prevention programs and cognitive diagnostic tools are appropriate strategies to reduce risk behaviors in mental health.

MiR-335-5p Inhibits β-Amyloid (Aβ) Accumulation to Attenuate Cognitive Deficits Through Targeting c-jun-N-terminal Kinase 3 in Alzheimer’s Disease

2020 ◽  
Vol 17 (1) ◽  
pp. 93-101 ◽  
Author(s):  
Dan Wang ◽  
Zhifu Fei ◽  
Song Luo ◽  
Hai Wang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Western Blot ◽  
Mrna Expression ◽  
Cognitive Deficits ◽  
Protein Levels ◽  
Amyloid Aβ ◽  
Β Amyloid ◽  
The Relationship

Objectives: Alzheimer's disease (AD), also known as senile dementia, is a common neurodegenerative disease characterized by progressive cognitive impairment and personality changes. Numerous evidences have suggested that microRNAs (miRNAs) are involved in the pathogenesis and development of AD. However, the exact role of miR-335-5p in the progression of AD is still not clearly clarified. Methods: The protein and mRNA levels were measured by western blot and RNA extraction and quantitative real-time PCR (qRT-PCR), respectively. The relationship between miR-335-5p and c-jun-N-terminal kinase 3 (JNK3) was confirmed by dual-luciferase reporter assay. SH-SY5Y cells were transfected with APP mutant gene to establish the in vitro AD cell model. Flow cytometry and western blot were performed to evaluate cell apoptosis. The APP/PS1 transgenic mice were used as an in vivo AD model. Morris water maze test was performed to assess the effect of miR- 335-5p on the cognitive deficits in APP/PS1 transgenic mice. Results: The JNK3 mRNA expression and protein levels of JNK3 and β-Amyloid (Aβ) were significantly up-regulated, and the mRNA expression of miR-335-5p was down-regulated in the brain tissues of AD patients. The expression levels of miR-335-5p and JNK3 were significantly inversely correlated. Further, the dual Luciferase assay verified the relationship between miR-335- 5p and JNK3. Overexpression of miR-335-5p significantly decreased the protein levels of JNK3 and Aβ and inhibited apoptosis in SH-SY5Y/APPswe cells, whereas the inhibition of miR-335-5p obtained the opposite results. Moreover, the overexpression of miR-335-5p remarkably improved the cognitive abilities of APP/PS1 mice. Conclusion: The results revealed that the increased JNK3 expression, negatively regulated by miR-335-5p, may be a potential mechanism that contributes to Aβ accumulation and AD progression, indicating a novel approach for AD treatment.

The nutritional consequences of foraging in primates: the relationship of nutrient intakes to nutrient requirements

1991 ◽  
Vol 334 (1270) ◽  
pp. 161-170 ◽  
Keyword(s):  
Food Selection ◽  
Nutrient Requirements ◽  
Nutrient Intakes ◽  
Protein Levels ◽  
Nutrient Density ◽  
High Nutrient ◽  
Relationship Of ◽  
The Relationship ◽  
High Dietary Protein ◽  
Growth And Reproduction

Many studies have examined the proportion of time that primates devote to feeding on various types of food, but relatively little is known about the intake rates associated with each food. However, the nutritional consequences of foraging can only be interpreted by comparing nutrient intakes with estimated nutrient requirements. The energy available to primates from ingested foods will depend both on the composition of the food and the extent to which various constituents, including fibre fractions, are digested. Both human and non-human primates have relatively low requirements for protein as a consequence of slow growth rates, small milk yields and relatively dilute milk. Because the nutrient demands of growth and reproduction are spread out over time, it appears that primates do not need to seek out foods of particularly high nutrient density, except perhaps during weaning. Although food selection in some species of primates appears to be correlated with the protein concentration of foods, it is unlikely that high dietary protein levels are required, at least when foods of balanced amino acid composition (such as leaves) are included in the diet.

New concepts on the structure of the neuronal networks: The miniaturization and hierarchical organization of the central nervous system*

1984 ◽  
Vol 4 (2) ◽  
pp. 93-98 ◽  
Author(s):  
Luigi F. Agnati ◽  
Kjell Fuxe
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neuronal Networks ◽  
Hierarchical Organization ◽  
Memory Storage ◽  
Information Handling ◽  
New Concepts ◽  
The Central Nervous System ◽  
Local Circuits ◽  
The Relationship

The hypothesis is introduced that miniaturization of neuronal circuits in the central nervous system and the hierarchical organization of the various levels, where information handling can take place, may be the key to understand the enormous capability of the human brain to store engrams as well as its astonishing capacity to reconstruct and organize engrams and thus to perform highly sophisticated integrations. The concept is also proposed that in order to understand the relationship between the structural and functional plasticity of the central nervous system it is necessary to postulate the existence of memory storage at the network level, at the local circuit level, at the synaptic level, at the membrane level, and finally at the molecular level. Thus, memory organization is similar to the hierarchical organization of the various levels, where information handling takes place in the nervous system. In addition, each higher level plays a role in the reconstruction and organization of the engrams stored at lower levels. Thus, the trace of the functionally stored memory (i.e. its reconstruction and organization at various levels of storage) will depend not only on the chemicophysical changes in the membranes of the local circuits but also on the organization of the local circuits themselves and their associated neuronal networks.

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