scholarly journals Bumble bee queens activate dopamine production and gene expression in nutritional signaling pathways in the brain

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ken Sasaki ◽  
Kakeru Yokoi ◽  
Kouhei Toga

AbstractTo explore the neuroendocrine mechanisms underlying caste-specific behavior and its evolution from primitive to advanced eusocial bees, the monoamine levels and expression of genes involved in monoamine production and signaling in the brain were compared between the castes of Bombus ignitus. Higher levels of dopamine and its related substances were found in the brains of newly emerged queens than in the brains of emerged workers. The degree of caste differences in B. ignitus was smaller than that reported in Apis mellifera, indicating a link to different social stages in the two species. There was no differential expression in genes involved in dopamine biosynthesis between castes, suggesting that the high dopamine production in queens was not largely influenced by the expression of these genes at emergence, rather it might be influenced by tyrosine supply. Genome-wide analyses of gene expression by RNA-sequencing indicated that a greater number of genes involved in nutrition were actively expressed in the brains of newly emerged queens in comparison to the emerged workers. Some of the expression was confirmed by real-time quantitative PCR. The signaling pathways driven by the expression of these genes may be associated with dopamine signaling or the parallel activation of dopamine production.

2021 ◽  
Vol 22 ◽  
Author(s):  
Vandana Golhani ◽  
Suman Kumar Ray ◽  
Sukhes Mukherjee

: MicroRNAs (miRNAs) and long non-coding RNAs (lncRNAs) are proficient in regulating gene expression post-transcriptionally. Considering the recent trend in exploiting non-coding RNAs (ncRNAs) as cancer therapeutics, the potential use of miRNAs and lncRNAs as biomarkers and novel therapeutic agents against angiogenesis is an important scientific aspect. An estimated 70% of the genome is actively transcribed, only 2% of which codes for known protein-coding genes. Long noncoding RNAs (lncRNAs) are a large and diverse class of RNAs > 200 nucleotides in length, and not translated into protein, and are of utmost importance and it governs the expression of genes in a temporal, spatial, and cell context-dependent manner. Angiogenesis is an essential process for organ morphogenesis and growth during development, and it is relevant during the repair of wounded tissue in adults. It is coordinated by an equilibrium of pro-and anti-angiogenic factors; nevertheless, when affected, it promotes several diseases, including breast cancer. Signaling pathways involved here are tightly controlled systems that regulate the appropriate timing of gene expression required for the differentiation of cells down a particular lineage essential for proper tissue development. Lately, scientific reports are indicating that ncRNAs, such as miRNAs, and lncRNAs, play critical roles in angiogenesis related to breast cancer. The specific roles of various miRNAs and lncRNAs in regulating angiogenesis in breast cancer, with particular focus on the downstream targets and signaling pathways regulated by these ncRNAs with molecular medicine perspective, are highlighted in this write-up.


2020 ◽  
Author(s):  
Brenda Cabrera-Mendoza

Despite individuals with substance use disorder (SUD) have a high suicide risk, most of gene expression studies in suicide have excluded individuals with this disorder. Thus, little is known about the gene expression profile in suicides with SUD. The identification of altered biological processes in the brain of suicides with SUD is crucial in the comprehension of the SUD and suicidal behavior comorbidity. This dissertation describes the evaluation of gene expression differences in the dorsolateral prefrontal cortex of suicides and non-suicides with and without SUD.Sixty-six brain tissue samples were collected and classified in the following groups: i) 23 suicides with SUD, ii) 20 suicides without SUD, iii) 9 non-suicides with SUD and iv) 14 non-suicides without SUD. The results of this study suggest that suicides with SUD have a gene expression profile in the prefrontal cortex different from that of individuals with only one of these conditions, presenting differences in the expression of genes involved in cell proliferation and glutamatergic neurotransmission.We performed a re-analysis of the gene expression data of 38 suicides focused on dual diagnosis and suicide. Dual diagnosis is the concurrence of at least one SUD and one or more mental disorders in a given individual. Although this comorbidity is highly prevalent and is associated with adverse clinical outcomes, its neurobiology has not been elucidated. In addition, patients with dual pathology have a higher suicide risk compared to patients with only one disorder.The objective of this re-analysis was to evaluate the differences in the gene expression profile in the prefrontal cortex of suicides with dual pathology compared to suicides with a single disorder. Our results suggest an alteration in the expression of genes involved in glutamatergic neurotransmission, GABAergic neurotransmission and neurogenesis in suicides with dual diagnosis compared to suicides with a single disorder and suicides without mental comorbidities.The observed differences in gene expression in the prefrontal cortex between suicides with and without SUD, as well as suicides with dual diagnosis and a single disorder may contribute to the phenotypic and clinical discrepancies observed among these patients. The identification of molecular characteristics in the brain of individuals with suicidal behavior and psychiatric comorbidities will allow the design of preventive and therapeutic measures aimed at the adequate treatment of each comorbidity.


2021 ◽  
Author(s):  
Weikang Cai ◽  
Xuemei Zhang ◽  
Thiago M. Batista ◽  
Rubén García-Martín ◽  
Samir Softic ◽  
...  

The brain is now recognized as an insulin sensitive tissue, however, the role of changing insulin concentrations in the peripheral circulation on gene expression in the brain is largely unknown. Here we perform hyperinsulinemic-euglycemic clamp on 3-month-old male C57BL/6 mice for 3 hours. We show that increases in peripheral insulin within the physiological range regulate expression of a broad network of gene expression in the brain compared with saline-infused controls. Insulin regulates distinct pathways in the hypothalamus, hippocampus and nucleus accumbens. Insulin shows its most robust effect in the hypothalamus and regulates multiple genes involved in neurotransmission, including up-regulating expression of multiple subunits of GABA-A receptors, Na<sup>+</sup> and K<sup>+</sup> channels, and SNARE proteins; differentially modulating glutamate receptors; and suppressing multiple neuropeptides. Insulin also strongly modulates metabolic genes in the hypothalamus, suppressing genes in the glycolysis and pentose phosphate pathways, while increasing expression of genes regulating pyruvate dehydrogenase and long-chain fatty acyl-CoA and cholesterol biosynthesis, thereby rerouting of carbon substrates from glucose metabolism to lipid metabolism required for the biogenesis of membranes for neuronal and glial function and synaptic remodeling. Furthermore, based on the transcriptional signatures, these changes in gene expression involve neurons, astrocytes, oligodendrocytes, microglia and endothelial cells. Thus, peripheral insulin acutely and potently regulates expression of a broad network of genes involved in neurotransmission and brain metabolism. Dysregulation of these pathways could have dramatic effects in normal physiology and diabetes.


2020 ◽  
Vol 103 (6) ◽  
pp. 1324-1335
Author(s):  
Albert J Thayil ◽  
Xuegeng Wang ◽  
Pooja Bhandari ◽  
Frederick S vom Saal ◽  
Donald E Tillitt ◽  
...  

Abstract Endocrine disrupting chemicals (EDCs), such as bisphenol A (BPA) and 17α-ethinylestradiol (EE2), can have far reaching health effects, including transgenerational abnormalities in offspring that never directly contacted either chemical. We previously reported reduced fertilization rates and embryo survival at F2 and F3 generations caused by 7-day embryonic exposure (F0) to 100 μg/L BPA or 0.05 μg/L EE2 in medaka. Crossbreeding of fish in F2 generation indicated subfertility in males. To further understand the mechanisms underlying BPA or EE2-induced adult onset and transgenerational reproductive defects in males, the present study examined the expression of genes regulating the brain–pituitary–testis (BPT) axis in the same F0 and F2 generation male medaka. Embryonic exposure to BPA or EE2 led to hyperactivation of brain and pituitary genes, which are actively involved in reproduction in adulthood of the F0 generation male fish, and some of these F0 effects continued to the F2 generation (transgenerational effects). Particularly, the F2 generation inherited the hyperactivated state of expression for kisspeptin (kiss1 and kiss2) and their receptors (kiss1r and kiss2r), and gnrh and gnrh receptors. At F2 generation, expression of DNA methyltransferase 1 (dnmt1) decreased in brain of the BPA treatment lineage, while EE2 treatment lineage showed increased dnmt3bb expression. Global hypomethylation pattern was observed in the testis of both F0 and F2 generation fish. Taken together, these results demonstrated that BPA or EE2-induced transgenerational reproductive impairment in the F2 generation was associated with alterations of reproductive gene expression in brain and testis and global DNA methylation in testis.


2021 ◽  
Vol 12 ◽  
Author(s):  
Venkatesh Chunduri ◽  
Amandeep Kaur ◽  
Shubhpreet Kaur ◽  
Aman Kumar ◽  
Saloni Sharma ◽  
...  

Recent weather fluctuations imposing heat stress at the time of wheat grain filling cause frequent losses in grain yield and quality. Field-based studies for understanding the effect of terminal heat stress on wheat are complicated by the effect of multiple confounding variables. In the present study, the effect of day and day–night combined heat stresses during the grain-filling stage was studied using gene expression and proteomics approaches. The gene expression analysis was performed by using real-time quantitative PCR (RT-qPCR). The expression of genes related to the starch biosynthetic pathway, starch transporters, transcription factors, and stress-responsive and storage proteins, at four different grain developmental stages, indicated the involvement of multiple pathways. Under the controlled conditions, their expression was observed until 28 days after anthesis (DAA). However, under the day stress and day–night stress, the expression of genes was initiated earlier and was observed until 14 DAA and 7 DAA, respectively. The protein profiles generated using two-dimensional polyacrylamide gel electrophoresis (2D-PAGE) and matrix-assisted laser desorption/ionization time-of-flight mass spectroscopy (MALDI-TOF MS/MS) showed a differential expression of the proteins belonging to multiple pathways that included the upregulation of proteins related to the translation, gliadins, and low-molecular-weight (LMW) glutenins and the downregulation of proteins related to the glycolysis, photosynthesis, defense, and high-molecular-weight (HMW) glutenins. Overall, the defense response to the day heat stress caused early gene expression and day–night heat stress caused suppression of gene expression by activating multiple pathways, which ultimately led to the reduction in grain-filling duration, grain weight, yield, and processing quality.


Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Tomoaki Aoki ◽  
Koichiro Shinozaki ◽  
Yu Okuma ◽  
Kei Hayashida ◽  
Ryosuke Takegawa ◽  
...  

Objective: We recently reported that post-resuscitation normoxic therapy attenuates oxidative stress in multiple organs and improves post-cardiac arrest (CA) organ injury, oxygen metabolism, and survival. Yet, detailed mechanisms of gene expression patterns and signaling pathways mitigated by normoxic therapy have not been elucidated. Therefore, we assessed post-resuscitation normoxic therapy-modified gene expression of oxidative stress-related signaling molecules. Methods: Rats were resuscitated from 10 minutes of asphyxial CA and divided into 2 groups: those that inhaled 100% supplemental O 2 (CA-FIO2 1.0) and those that inhaled 30% supplemental O 2 (CA-FIO2 0.3). Control groups were also prepared for comparison (control-FIO2 1.0, control-FIO2 0.3). At 2 hours after resuscitation, brain and heart tissues were collected, and mRNA purifications followed by real-time PCR measurements were performed to compare gene expression of hyperoxia-induced inflammatory and apoptosis-related signaling pathways amongst these groups. Results: In the brain, relative IL-1 beta mRNA gene expression levels, which represent inflammatory signaling pathways, increased post-CA (8.1±2.3 in CA-FIO2 1.0 and 1.0±0.4 in control-FIO2 0.3, p<0.05), but were significantly attenuated by normoxic therapy (2.3±0.2 in CA-FIO2 0.3, p<0.05). Likewise, normoxic therapy significantly reduced oxidative stress-induced inflammatory (NFKB1, TGFB1, MAPK14, TRAF6) and apoptosis-related (BAX, EGF) mRNA gene expression levels in the brain, whereas no statistical differences were detected in the heart. Conclusions: Post-CA normoxic therapy significantly attenuated the gene expression of oxidative stress-induced inflammation and apoptosis in the brain, while there were no remarkable changes in the heart. Therefore, it is inferred that the heart is more tolerant to hyperoxic injury compared to the brain.


2018 ◽  
Vol 115 (33) ◽  
pp. 8442-8447 ◽  
Author(s):  
Fabián E. Vaistij ◽  
Thiago Barros-Galvão ◽  
Adama F. Cole ◽  
Alison D. Gilday ◽  
Zhesi He ◽  
...  

Seed germination in many plant species is triggered by sunlight, which is rich in the red (R) wavelength and repressed by under-the-canopy light rich in far red (FR). R:FR ratios are sensed by phytochromes to regulate levels of gibberellins (GAs) and abscisic acid (ABA), which induce and inhibit germination respectively. In this study we have discovered that, under FR light conditions, germination is repressed by MOTHER-OF-FT-AND-TFL1 (MFT) through the regulation of the ABA and GA signaling pathways. We also show that MFT gene expression is tightly regulated by light quality. Previous work has shown that under FR light conditions the transcription factor PHYOCHROME-INTERACTING-FACTOR1 (PIF1) accumulates and promotes expression of SOMNUS (SOM) that, in turn, leads to increased ABA and decreased GA levels. PIF1 also promotes expression of genes encoding ABA-INSENSITIVE5 (ABI5) and DELLA growth-repressor proteins, which act in the ABA and GA signaling pathways, respectively. Here we show that MFT gene expression is promoted by FR light through the PIF1/SOM/ABI5/DELLA pathway and is repressed by R light via the transcription factor SPATULA (SPT). Consistent with this, we also show that SPT gene expression is repressed under FR light in a PIF1-dependent manner. Furthermore, transcriptomic analyses presented in this study indicate that MFT exerts its function by promoting expression of known ABA-induced genes and repressing cell wall expansion-related genes.


2021 ◽  
Author(s):  
Weikang Cai ◽  
Xuemei Zhang ◽  
Thiago M. Batista ◽  
Rubén García-Martín ◽  
Samir Softic ◽  
...  

The brain is now recognized as an insulin sensitive tissue, however, the role of changing insulin concentrations in the peripheral circulation on gene expression in the brain is largely unknown. Here we perform hyperinsulinemic-euglycemic clamp on 3-month-old male C57BL/6 mice for 3 hours. We show that increases in peripheral insulin within the physiological range regulate expression of a broad network of gene expression in the brain compared with saline-infused controls. Insulin regulates distinct pathways in the hypothalamus, hippocampus and nucleus accumbens. Insulin shows its most robust effect in the hypothalamus and regulates multiple genes involved in neurotransmission, including up-regulating expression of multiple subunits of GABA-A receptors, Na<sup>+</sup> and K<sup>+</sup> channels, and SNARE proteins; differentially modulating glutamate receptors; and suppressing multiple neuropeptides. Insulin also strongly modulates metabolic genes in the hypothalamus, suppressing genes in the glycolysis and pentose phosphate pathways, while increasing expression of genes regulating pyruvate dehydrogenase and long-chain fatty acyl-CoA and cholesterol biosynthesis, thereby rerouting of carbon substrates from glucose metabolism to lipid metabolism required for the biogenesis of membranes for neuronal and glial function and synaptic remodeling. Furthermore, based on the transcriptional signatures, these changes in gene expression involve neurons, astrocytes, oligodendrocytes, microglia and endothelial cells. Thus, peripheral insulin acutely and potently regulates expression of a broad network of genes involved in neurotransmission and brain metabolism. Dysregulation of these pathways could have dramatic effects in normal physiology and diabetes.


2020 ◽  
Author(s):  
Trieu-Duc Vu ◽  
Yuki Iwasaki ◽  
Kenshiro Oshima ◽  
Masato Nikaido ◽  
Ming-Tzu Chiu ◽  
...  

AbstractTerritorial defense involves frequent aggressive confrontations with competitors, but little is known about how brain-transcriptomic profiles change between individuals competing for territory establishment. Our previous study elucidated that brain-transcriptomic synchronization occurs in a pair-specific manner between two males of the fish Betta splendens during fighting, reflecting a mutual assessment process between them at the level of gene expression. Here we evaluated how the brain-transcriptomic profiles of opponents change immediately after shifting their social status (i.e., the winner/loser has emerged) and 30 min after this shift. We showed that unique and carryover hypotheses can be adapted to this system, in which changes in the expression of certain genes are unique to different fighting stages and in which the expression patterns of certain genes are transiently or persistently changed across all fighting stages. Interestingly, the specificity of the brain-transcriptomic synchronization of a pair during fighting was gradually lost after fighting ceased, because of the decrease in the variance in gene expression across all individuals, leading to the emergence of a basal neurogenomic state. Strikingly, this unique state was more basal than the state that existed in the before-fighting group and resulted in the reduced and consistent expression of genes across all individuals. In spite of the consistent and basal overall gene expression in each individual in this state, expression changes for genes related to metabolism, learning and memory, and autism still differentiated losers from winners. The fighting system using male B. splendens thus provides a promising platform for investigating neurogenomic states of aggression in vertebrates.Author summaryCompetitive interactions involve complex decision-making tasks that are shaped by mutual feedback between participants. When two animals interact, transcriptomes across their brains synchronize in a way that reflects how they assess and predict the other’s fighting ability and react to each other’s decisions. Here, we elucidated the gradual loss of brain-transcriptomic synchrony between interacting opponents after their interaction ceased, leading to the emergence of a basal neurogenomic state, in which the variations in gene expression were reduced to a minimum among all individuals. This basal neurogenomic state shares common characteristics with the hibernation state, which animals adopt to minimize their metabolic rates to cope with harsh environmental conditions. We demonstrated that this unique neurogenomic state, which is newly characterized in the present study, is composed of the expression of a unique set of genes, each of which was presumably minimally required for survival, providing a hypothesis that this state represents the smallest unit of neurogenomic activity for sustaining an active life.


2020 ◽  
Vol 21 (10) ◽  
pp. 3566 ◽  
Author(s):  
Sung Wook Kim ◽  
Kyong-Tai Kim

Neuronal axons are guided to their target during the development of the brain. Axon guidance allows the formation of intricate neural circuits that control the function of the brain, and thus the behavior. As the axons travel in the brain to find their target, they encounter various axon guidance cues, which interact with the receptors on the tip of the growth cone to permit growth along different signaling pathways. Although many scientists have performed numerous studies on axon guidance signaling pathways, we still have an incomplete understanding of the axon guidance system. Lately, studies on axon guidance have shifted from studying the signal transduction pathways to studying other molecular features of axon guidance, such as the gene expression. These new studies present evidence for different molecular features that broaden our understanding of axon guidance. Hence, in this review we will introduce recent studies that illustrate different molecular features of axon guidance. In particular, we will review literature that demonstrates how axon guidance cues and receptors regulate local translation of axonal genes and how the expression of guidance cues and receptors are regulated both transcriptionally and post-transcriptionally. Moreover, we will highlight the pathological relevance of axon guidance molecules to specific diseases.


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