首页 > 最新文献

Journal of neurogenetics最新文献

英文 中文
Neural stem cell-derived exosomal FTO protects neuron from microglial inflammatory injury by inhibiting microglia NRF2 mRNA m6A modification. 神经干细胞来源的外泌体FTO通过抑制小胶质细胞NRF2 mRNA m6A修饰来保护神经元免受小胶质细胞炎症损伤。
IF 1.9 4区 医学 Q3 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-09-01 Epub Date: 2023-10-16 DOI: 10.1080/01677063.2023.2259995
Zhiyong Li, Zhenggang Chen, Jun Peng

Ischemic stroke (IS) can cause neuronal cell loss and function defects. Exosomes derived from neural stem cells (NSC-Exos) improve neural plasticity and promote neural function repair following IS. However, the potential mechanism remains unclear. In this study, NSC-Exos were characterized and co-cultured with microglia. We found that NSC-Exos increased NRF2 expression in oxygen-glucose deprivation/reoxygenation and LPS-induced microglia and converted microglia from M1 pro-inflammatory phenotype to M2 anti-inflammatory phenotype. NSC-Exos reduced m6A methylation modification of nuclear factor erythroid 2-related factor 2 (NRF2) mRNA via obesity-associated gene (FTO). Furthermore, NSC-Exos reduced the damage to neurons caused by microglia's inflammatory response. Finally, the changes in microglia polarization and neuron damage caused by FTO knockdown in NSE-Exos were attenuated by NRF2 overexpression in microglia. These findings revealed that NSC-Exos promotes NRF2 expression and M2 polarization of microglial via transferring FTO, thereby resulting in neuroprotective effects.

缺血性中风(IS)可导致神经元细胞损失和功能缺陷。来源于神经干细胞的外泌体(NSC-Exos)改善IS后的神经可塑性并促进神经功能修复。然而,其潜在机制尚不清楚。本研究对NSC外显子进行了表征,并与小胶质细胞共培养。我们发现NSC-Exos在氧-葡萄糖剥夺/复氧和LPS诱导的小胶质细胞中增加了NRF2的表达,并将小胶质细胞从M1促炎表型转化为M2抗炎表型。NSC-Exos通过肥胖相关基因(FTO)减少核因子红系2相关因子2(NRF2)mRNA的m6A甲基化修饰。此外,NSC-Exos减少了小胶质细胞炎症反应对神经元的损伤。最后,小胶质细胞中NRF2过表达减弱了由NSE Exos中FTO敲低引起的小胶质细胞极化和神经元损伤的变化。这些发现表明,NSC-Exos通过转移FTO促进小胶质细胞的NRF2表达和M2极化,从而产生神经保护作用。
{"title":"Neural stem cell-derived exosomal FTO protects neuron from microglial inflammatory injury by inhibiting microglia NRF2 mRNA m6A modification.","authors":"Zhiyong Li, Zhenggang Chen, Jun Peng","doi":"10.1080/01677063.2023.2259995","DOIUrl":"10.1080/01677063.2023.2259995","url":null,"abstract":"<p><p>Ischemic stroke (IS) can cause neuronal cell loss and function defects. Exosomes derived from neural stem cells (NSC-Exos) improve neural plasticity and promote neural function repair following IS. However, the potential mechanism remains unclear. In this study, NSC-Exos were characterized and co-cultured with microglia. We found that NSC-Exos increased NRF2 expression in oxygen-glucose deprivation/reoxygenation and LPS-induced microglia and converted microglia from M1 pro-inflammatory phenotype to M2 anti-inflammatory phenotype. NSC-Exos reduced m6A methylation modification of nuclear factor erythroid 2-related factor 2 (NRF2) mRNA via obesity-associated gene (FTO). Furthermore, NSC-Exos reduced the damage to neurons caused by microglia's inflammatory response. Finally, the changes in microglia polarization and neuron damage caused by FTO knockdown in NSE-Exos were attenuated by NRF2 overexpression in microglia. These findings revealed that NSC-Exos promotes NRF2 expression and M2 polarization of microglial via transferring FTO, thereby resulting in neuroprotective effects.</p>","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":null,"pages":null},"PeriodicalIF":1.9,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41133141","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The DST gene in neurobiology. 神经生物学中的 DST 基因
IF 1.9 4区 医学 Q3 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-09-01 Epub Date: 2024-03-11 DOI: 10.1080/01677063.2024.2319880
Robert Lalonde, Catherine Strazielle

DST is a gene whose alternative splicing yields epithelial, neuronal, and muscular isoforms. The autosomal recessive Dstdt (dystonia musculorum) spontaneous mouse mutation causes degeneration of spinocerebellar tracts as well as peripheral sensory nerves, dorsal root ganglia, and cranial nerve ganglia. In addition to Dstdt mutants, axonopathy and neurofilament accumulation in perikarya are features of two other murine lines with spontaneous Dst mutations, targeted Dst knockout mice, DstTg4 transgenic mice carrying two deleted Dst exons, DstGt mice with trapped actin-binding domain-containing isoforms, and conditional Schwann cell-specific Dst knockout mice. As a result of nerve damage, Dstdt mutants display dystonia and ataxia, as seen in several genetically modified models and their motor coordination deficits have been quantified along with the spontaneous Dst nonsense mutant, the conditional Schwann cell-specific Dst knockout, the conditional DstGt mutant, and the Dst-b isoform specific Dst mutant. Recent findings in humans have associated DST mutations of the Dst-b isoform with hereditary sensory and autonomic neuropathies type 6 (HSAN-VI). These data should further encourage the development of genetic techniques to treat or prevent ataxic and dystonic symptoms.

DST 是一种基因,其替代剪接可产生上皮细胞、神经细胞和肌肉异构体。常染色体隐性遗传的 Dstdt(肌张力障碍)小鼠自发突变会导致脊髓小脑束以及周围感觉神经、背根神经节和颅神经节变性。除 Dstdt 突变体外,轴突病变和神经纤维在神经周围积聚也是其他两个自发性 Dst 突变小鼠品系、靶向 Dst 基因敲除小鼠、携带两个缺失 Dst 外显子的 DstTg4 转基因小鼠、含有肌动蛋白结合域异构体的 DstGt 小鼠和条件性许旺细胞特异性 Dst 基因敲除小鼠的特征。由于神经损伤,Dstdt 突变体表现出肌张力障碍和共济失调,这在几种转基因模型中都可以看到,而且它们的运动协调障碍已经与自发性 Dst 无义突变体、条件性许旺细胞特异性 Dst 基因敲除、条件性 DstGt 突变体和 Dst-b 异构体特异性 Dst 突变体一起进行了量化。最近的人类研究发现,Dst-b 同工型的 DST 突变与遗传性感觉和自主神经病变 6 型(HSAN-VI)有关。这些数据将进一步促进治疗或预防共济失调和肌张力障碍症状的基因技术的发展。
{"title":"The <i>DST</i> gene in neurobiology.","authors":"Robert Lalonde, Catherine Strazielle","doi":"10.1080/01677063.2024.2319880","DOIUrl":"10.1080/01677063.2024.2319880","url":null,"abstract":"<p><p><i>DST</i> is a gene whose alternative splicing yields epithelial, neuronal, and muscular isoforms. The autosomal recessive <i>Dst<sup>dt</sup></i> (<i>dystonia musculorum</i>) spontaneous mouse mutation causes degeneration of spinocerebellar tracts as well as peripheral sensory nerves, dorsal root ganglia, and cranial nerve ganglia. In addition to <i>Dst<sup>dt</sup></i> mutants, axonopathy and neurofilament accumulation in perikarya are features of two other murine lines with spontaneous <i>Dst</i> mutations, targeted <i>Dst</i> knockout mice, <i>Dst</i>Tg4 transgenic mice carrying two deleted <i>Dst</i> exons, <i>Dst</i><sup>Gt</sup> mice with trapped actin-binding domain-containing isoforms, and conditional Schwann cell-specific <i>Dst</i> knockout mice. As a result of nerve damage, <i>Dst<sup>dt</sup></i> mutants display dystonia and ataxia, as seen in several genetically modified models and their motor coordination deficits have been quantified along with the spontaneous <i>Dst</i> nonsense mutant, the conditional Schwann cell-specific <i>Dst</i> knockout, the conditional <i>Dst</i><sup>Gt</sup> mutant, and the Dst-b isoform specific <i>Dst</i> mutant. Recent findings in humans have associated <i>DST</i> mutations of the Dst-b isoform with hereditary sensory and autonomic neuropathies type 6 (HSAN-VI). These data should further encourage the development of genetic techniques to treat or prevent ataxic and dystonic symptoms.</p>","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":null,"pages":null},"PeriodicalIF":1.9,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140094230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Yin Yang 1 suppresses apoptosis and oxidative stress injury in SH-SY5Y cells by facilitating NR4A1 expression. 阴阳1号通过促进NR4A1的表达来抑制SH-SY5Y细胞的凋亡和氧化应激损伤。
IF 1.9 4区 医学 Q3 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-09-01 Epub Date: 2023-11-03 DOI: 10.1080/01677063.2023.2270745
Qin Kang, Wen Chai, Jun Min, Xinhui Qu

Oxidative stress plays a significant role in the development of Parkinson's disease (PD). Previous studies implicate nuclear receptor subfamily 4 group A member 1 (NR4A1) in oxidative stress associated with PD. However, the molecular mechanism underlying the regulation of NR4A1 expression remains incompletely understood. In the present study, a PD cell model was established by using 1-methyl-4-phenylpyridinium (MPP+) in SH-SY5Y cells. Cell viability and apoptosis were assessed by using CCK-8 assay and flow cytometry, respectively. The activities of LDH and SOD, and ROS generation were used as an indicators of oxidative stress. ChIP-PCR was performed to detect the interaction between Yin Yang 1 (YY1) and the NR4A1 promoter. MPP+ treatment inhibited SH-SY5Y cell viability in a dose- and time-dependent manner. NR4A1 and YY1 expression were decreased in MPP+-treated SH-SY5Y cells. Increasing NR4A1 or YY1 alleviated MPP+-induced apoptosis and oxidative stress in SH-SY5Y cells, whereas reduction of NR4A1 aggravated MPP+-induced cell injury. Transcription factor YY1 facilitated NR4A1 expression by binding with NR4A1 promoter. In addition, in MPP+-treated SH-SY5Y cells, the inhibition of NR4A1 to apoptosis and oxidative stress was further enhanced by overexpression of YY1. The reduction of NR4A1 led to an elevation of apoptosis and oxidative stress in MPP+-induced SH-SY5Y cells, and this effect was partially reversed by the overexpression of YY1. In conclusion, YY1 suppresses MPP+-induced apoptosis and oxidative stress in SH-SY5Y cells by binding with NR4A1 promoter and boosting NR4A1 expression. Our findings suggest that NR4A1 may be a candidate target for PD treatment.HIGHLIGHTSNR4A1 and YY1 are decreased in MPP+-treated SH-SY5Y cells.NR4A1 prevents oxidative stress and apoptosis in MPP+-treated SH-SY5Y cells.YY1 binds with NR4A1 promoter and increases NR4A1 expression.YY1 enhances the inhibition of NR4A1 to SH-SY5Y cell apoptosis and oxidative stress.

氧化应激在帕金森病(PD)的发展中起着重要作用。先前的研究表明,核受体亚家族4 A组成员1(NR4A1)与PD相关的氧化应激有关。然而,NR4A1表达调控的分子机制尚不完全清楚。在本研究中,通过在SH-SY5Y细胞中使用1-甲基-4-苯基吡啶鎓(MPP+)建立PD细胞模型。分别用CCK-8法和流式细胞术评估细胞活力和细胞凋亡。LDH和SOD的活性以及ROS的产生被用作氧化应激的指标。ChIP-PCR检测阴阳1(YY1)与NR4A1启动子之间的相互作用。MPP+处理以剂量和时间依赖的方式抑制SH-SY5Y细胞的活力。NR4A1和YY1在MPP+处理的SH-SY5Y细胞中的表达降低。增加NR4A1或YY1可减轻MPP+诱导的SH-SY5Y细胞凋亡和氧化应激,而减少NR4A1可加重MPP+诱发的细胞损伤。转录因子YY1通过与NR4A1启动子结合促进NR4A1的表达。此外,在MPP+处理的SH-SY5Y细胞中,YY1的过表达进一步增强了NR4A1对细胞凋亡和氧化应激的抑制作用。NR4A1的减少导致MPP+诱导的SH-SY5Y细胞中细胞凋亡和氧化应激的升高,YY1的过表达部分逆转了这种作用。总之,YY1通过与NR4A1启动子结合并促进NR4A1的表达来抑制MPP+诱导的SH-SY5Y细胞的凋亡和氧化应激。我们的研究结果表明,NR4A1可能是PD治疗的候选靶点。HIGHGHGHTSNR4A1和YY1在MPP+处理的SH-SY5Y细胞中降低。NR4A1在MPP+处理的SH-SY5Y细胞中防止氧化应激和细胞凋亡。YY1与NR4A1启动子结合并增加NR4A1的表达。YY1增强NR4A1对SH-SY5Y细胞凋亡和氧化应激的抑制作用。
{"title":"Yin Yang 1 suppresses apoptosis and oxidative stress injury in SH-SY5Y cells by facilitating NR4A1 expression.","authors":"Qin Kang, Wen Chai, Jun Min, Xinhui Qu","doi":"10.1080/01677063.2023.2270745","DOIUrl":"10.1080/01677063.2023.2270745","url":null,"abstract":"<p><p>Oxidative stress plays a significant role in the development of Parkinson's disease (PD). Previous studies implicate nuclear receptor subfamily 4 group A member 1 (NR4A1) in oxidative stress associated with PD. However, the molecular mechanism underlying the regulation of NR4A1 expression remains incompletely understood. In the present study, a PD cell model was established by using 1-methyl-4-phenylpyridinium (MPP<sup>+</sup>) in SH-SY5Y cells. Cell viability and apoptosis were assessed by using CCK-8 assay and flow cytometry, respectively. The activities of LDH and SOD, and ROS generation were used as an indicators of oxidative stress. ChIP-PCR was performed to detect the interaction between Yin Yang 1 (YY1) and the <i>NR4A1</i> promoter. MPP<sup>+</sup> treatment inhibited SH-SY5Y cell viability in a dose- and time-dependent manner. NR4A1 and YY1 expression were decreased in MPP<sup>+</sup>-treated SH-SY5Y cells. Increasing NR4A1 or YY1 alleviated MPP<sup>+</sup>-induced apoptosis and oxidative stress in SH-SY5Y cells, whereas reduction of NR4A1 aggravated MPP<sup>+</sup>-induced cell injury. Transcription factor YY1 facilitated NR4A1 expression by binding with <i>NR4A1</i> promoter. In addition, in MPP<sup>+</sup>-treated SH-SY5Y cells, the inhibition of NR4A1 to apoptosis and oxidative stress was further enhanced by overexpression of YY1. The reduction of NR4A1 led to an elevation of apoptosis and oxidative stress in MPP<sup>+</sup>-induced SH-SY5Y cells, and this effect was partially reversed by the overexpression of YY1. In conclusion, YY1 suppresses MPP<sup>+</sup>-induced apoptosis and oxidative stress in SH-SY5Y cells by binding with <i>NR4A1</i> promoter and boosting NR4A1 expression. Our findings suggest that NR4A1 may be a candidate target for PD treatment.HIGHLIGHTSNR4A1 and YY1 are decreased in MPP<sup>+</sup>-treated SH-SY5Y cells.NR4A1 prevents oxidative stress and apoptosis in MPP<sup>+</sup>-treated SH-SY5Y cells.YY1 binds with <i>NR4A1</i> promoter and increases NR4A1 expression.YY1 enhances the inhibition of NR4A1 to SH-SY5Y cell apoptosis and oxidative stress.</p>","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":null,"pages":null},"PeriodicalIF":1.9,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71434299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
A conserved function of Pkhd1l1, a mammalian hair cell stereociliary coat protein, in regulating hearing in zebrafish. 哺乳动物毛细胞立体纤毛外壳蛋白Pkhd1l1在调节斑马鱼听力中的保守功能。
IF 1.9 4区 医学 Q3 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-09-01 Epub Date: 2023-03-24 DOI: 10.1080/01677063.2023.2187792
Stylianos Makrogkikas, Ruey-Kuang Cheng, Hao Lu, Sudipto Roy

Pkhd1l1 is predicted to encode a very large type-I transmembrane protein, but its function has largely remained obscure. Recently, it was shown that Pkhdl1l1 is a component of the coat that decorates stereocilia of outer hair cells in the mouse ear. Consistent with this localization, conditional deletion of Pkhd1l1 specifically from hair cells, was associated with progressive hearing loss. In the zebrafish, there are two paralogous pkhd1l1 genes - pkhd1l1α and pkhd1l1β. Using CRISPR-Cas9 mediated gene editing, we generated loss-of-function alleles for both and show that the double mutants exhibit nonsense-mediated-decay (NMD) of the RNAs. With behavioural assays, we demonstrate that zebrafish pkhd1l1 genes also regulate hearing; however, in contrast to Pkhd1l1 mutant mice, which develop progressive hearing loss, the double mutant zebrafish exhibited statistically significant hearing loss even from the larval stage. Our data highlight a conserved function of Pkhd1l1 in hearing and based on these findings from animal models, we postulate that PKHD1L1 could be a candidate gene for sensorineural hearing loss (SNHL) in humans.

Pkhd1l1被预测编码一种非常大的I型跨膜蛋白,但其功能在很大程度上仍不清楚。最近,研究表明,Pkhdl1l1是装饰小鼠耳朵外毛细胞立体纤毛的外壳的一种成分。与这种定位一致的是,有条件地从毛细胞中特异性地缺失Pkhd1l1与进行性听力损失有关。在斑马鱼中,有两个同源的pkhd1l1基因——pkhd1llα和pkhd1lβ。使用CRISPR-Cas9介导的基因编辑,我们产生了两者的功能缺失等位基因,并表明双突变体表现出RNA的无义介导衰变(NMD)。通过行为分析,我们证明斑马鱼pkhd1l1基因也调节听力;然而,与出现进行性听力损失的Pkhd1l1突变小鼠相比,双突变斑马鱼甚至从幼虫阶段就表现出统计学上显著的听力损失。我们的数据强调了Pkhd1l1在听力中的保守功能,基于动物模型的这些发现,我们推测Pkhd1l1可能是人类感音神经性听力损失(SNHL)的候选基因。
{"title":"A conserved function of Pkhd1l1, a mammalian hair cell stereociliary coat protein, in regulating hearing in zebrafish.","authors":"Stylianos Makrogkikas,&nbsp;Ruey-Kuang Cheng,&nbsp;Hao Lu,&nbsp;Sudipto Roy","doi":"10.1080/01677063.2023.2187792","DOIUrl":"10.1080/01677063.2023.2187792","url":null,"abstract":"<p><p><i>Pkhd1l1</i> is predicted to encode a very large type-I transmembrane protein, but its function has largely remained obscure. Recently, it was shown that Pkhdl1l1 is a component of the coat that decorates stereocilia of outer hair cells in the mouse ear. Consistent with this localization, conditional deletion of <i>Pkhd1l1</i> specifically from hair cells, was associated with progressive hearing loss. In the zebrafish, there are two paralogous <i>pkhd1l1</i> genes - <i>pkhd1l1α</i> and <i>pkhd1l1β.</i> Using CRISPR-Cas9 mediated gene editing, we generated loss-of-function alleles for both and show that the double mutants exhibit nonsense-mediated-decay (NMD) of the RNAs. With behavioural assays, we demonstrate that zebrafish <i>pkhd1l1</i> genes also regulate hearing; however, in contrast to <i>Pkhd1l1</i> mutant mice, which develop progressive hearing loss, the double mutant zebrafish exhibited statistically significant hearing loss even from the larval stage. Our data highlight a conserved function of <i>Pkhd1l1</i> in hearing and based on these findings from animal models, we postulate that <i>PKHD1L1</i> could be a candidate gene for sensorineural hearing loss (SNHL) in humans.</p>","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":null,"pages":null},"PeriodicalIF":1.9,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9240088","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Starvation-induced sleep suppression requires the Drosophila brain nutrient sensor. 饥饿引起的睡眠抑制需要果蝇的大脑营养传感器。
IF 1.9 4区 医学 Q3 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-03-01 DOI: 10.1080/01677063.2023.2203489
Yangkyun Oh, Greg S B Suh

Animals increase their locomotion activity and reduce sleep duration under starved conditions. This suggests that sleep and metabolic status are closely interconnected. The nutrient and hunger sensors in the Drosophila brain, including diuretic hormone 44 (DH44)-, CN-, and cupcake-expressing neurons, detect circulating glucose levels in the internal milieu, regulate the insulin and glucagon secretion and promote food consumption. Food deprivation is known to reduce sleep duration, but a potential role mediated by the nutrient and hunger sensors in regulating sleep and locomotion activity remains unclear. Here, we show that DH44 neurons are involved in regulating starvation-induced sleep suppression, but CN neurons or cupcake neurons may not be involved in regulating starvation-induced sleep suppression or baseline sleep patterns. Inactivation of DH44 neurons resulted in normal daily sleep durations and patterns under fed conditions, whereas it ablated sleep reduction under starved conditions. Inactivation of CN neurons or cupcake neurons, which were proposed to be nutrient and hunger sensors in the fly brain, did not affect sleep patterns under both fed and starved conditions. We propose that the glucose-sensing DH44 neurons play an important role in mediating starvation-induced sleep reduction.

动物在饥饿的情况下会增加运动活动,减少睡眠时间。这表明睡眠和代谢状态是密切相关的。果蝇大脑中的营养和饥饿传感器,包括利尿激素44 (DH44)-、CN-和表达纸杯蛋糕的神经元,检测内部环境中的循环葡萄糖水平,调节胰岛素和胰高血糖素的分泌,促进食物消耗。已知食物剥夺会减少睡眠时间,但营养和饥饿传感器在调节睡眠和运动活动中的潜在作用尚不清楚。在这里,我们发现DH44神经元参与调节饥饿诱导的睡眠抑制,但CN神经元或纸杯蛋糕神经元可能不参与调节饥饿诱导的睡眠抑制或基线睡眠模式。在进食条件下,DH44神经元的失活导致正常的日常睡眠时间和模式,而在饥饿条件下,它会减少睡眠。CN神经元或纸杯蛋糕神经元被认为是果蝇大脑中的营养和饥饿传感器,它们的失活在喂食和饥饿条件下都不会影响睡眠模式。我们认为葡萄糖感知DH44神经元在介导饥饿引起的睡眠减少中起重要作用。
{"title":"Starvation-induced sleep suppression requires the <i>Drosophila</i> brain nutrient sensor.","authors":"Yangkyun Oh,&nbsp;Greg S B Suh","doi":"10.1080/01677063.2023.2203489","DOIUrl":"https://doi.org/10.1080/01677063.2023.2203489","url":null,"abstract":"<p><p>Animals increase their locomotion activity and reduce sleep duration under starved conditions. This suggests that sleep and metabolic status are closely interconnected. The nutrient and hunger sensors in the <i>Drosophila</i> brain, including diuretic hormone 44 (DH44)-, CN-, and cupcake-expressing neurons, detect circulating glucose levels in the internal milieu, regulate the insulin and glucagon secretion and promote food consumption. Food deprivation is known to reduce sleep duration, but a potential role mediated by the nutrient and hunger sensors in regulating sleep and locomotion activity remains unclear. Here, we show that DH44 neurons are involved in regulating starvation-induced sleep suppression, but CN neurons or cupcake neurons may not be involved in regulating starvation-induced sleep suppression or baseline sleep patterns. Inactivation of DH44 neurons resulted in normal daily sleep durations and patterns under fed conditions, whereas it ablated sleep reduction under starved conditions. Inactivation of CN neurons or cupcake neurons, which were proposed to be nutrient and hunger sensors in the fly brain, did not affect sleep patterns under both fed and starved conditions. We propose that the glucose-sensing DH44 neurons play an important role in mediating starvation-induced sleep reduction.</p>","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":null,"pages":null},"PeriodicalIF":1.9,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10171511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
A deep learning analysis of Drosophila body kinematics during magnetically tethered flight. 果蝇在磁系飞行过程中身体运动学的深度学习分析。
IF 1.9 4区 医学 Q3 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-03-01 DOI: 10.1080/01677063.2023.2210682
Geonil Kim, JoonHu An, Subin Ha, Anmo J Kim

Flying Drosophila rely on their vision to detect visual objects and adjust their flight course. Despite their robust fixation on a dark, vertical bar, our understanding of the underlying visuomotor neural circuits remains limited, in part due to difficulties in analyzing detailed body kinematics in a sensitive behavioral assay. In this study, we observed the body kinematics of flying Drosophila using a magnetically tethered flight assay, in which flies are free to rotate around their yaw axis, enabling naturalistic visual and proprioceptive feedback. Additionally, we used deep learning-based video analyses to characterize the kinematics of multiple body parts in flying animals. By applying this pipeline of behavioral experiments and analyses, we characterized the detailed body kinematics during rapid flight turns (or saccades) in two different visual conditions: spontaneous flight saccades under static screen and bar-fixating saccades while tracking a rotating bar. We found that both types of saccades involved movements of multiple body parts and that the overall dynamics were comparable. Our study highlights the importance of sensitive behavioral assays and analysis tools for characterizing complex visual behaviors.

果蝇依靠它们的视觉来探测视觉物体并调整它们的飞行路线。尽管他们牢固地固定在一个黑暗的垂直条上,我们对潜在的视觉运动神经回路的理解仍然有限,部分原因是难以在敏感的行为分析中分析详细的身体运动学。在这项研究中,我们使用磁系飞行实验观察飞行果蝇的身体运动学,其中苍蝇可以围绕其偏航轴自由旋转,从而实现自然的视觉和本体感觉反馈。此外,我们使用基于深度学习的视频分析来表征飞行动物多个身体部位的运动学。通过应用这些行为实验和分析,我们在两种不同的视觉条件下描述了快速飞行转弯(或扫视)时的详细身体运动学:静态屏幕下的自发飞行扫视和跟踪旋转杆时注视杆的扫视。我们发现,两种类型的扫视都涉及到多个身体部位的运动,而且总体动态是相似的。我们的研究强调了敏感的行为分析和分析工具对表征复杂视觉行为的重要性。
{"title":"A deep learning analysis of <i>Drosophila</i> body kinematics during magnetically tethered flight.","authors":"Geonil Kim,&nbsp;JoonHu An,&nbsp;Subin Ha,&nbsp;Anmo J Kim","doi":"10.1080/01677063.2023.2210682","DOIUrl":"https://doi.org/10.1080/01677063.2023.2210682","url":null,"abstract":"<p><p>Flying <i>Drosophila</i> rely on their vision to detect visual objects and adjust their flight course. Despite their robust fixation on a dark, vertical bar, our understanding of the underlying visuomotor neural circuits remains limited, in part due to difficulties in analyzing detailed body kinematics in a sensitive behavioral assay. In this study, we observed the body kinematics of flying <i>Drosophila</i> using a magnetically tethered flight assay, in which flies are free to rotate around their yaw axis, enabling naturalistic visual and proprioceptive feedback. Additionally, we used deep learning-based video analyses to characterize the kinematics of multiple body parts in flying animals. By applying this pipeline of behavioral experiments and analyses, we characterized the detailed body kinematics during rapid flight turns (or saccades) in two different visual conditions: spontaneous flight saccades under static screen and bar-fixating saccades while tracking a rotating bar. We found that both types of saccades involved movements of multiple body parts and that the overall dynamics were comparable. Our study highlights the importance of sensitive behavioral assays and analysis tools for characterizing complex visual behaviors.</p>","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":null,"pages":null},"PeriodicalIF":1.9,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9784307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
Reduced branched-chain aminotransferase activity alleviates metabolic vulnerability caused by dim light exposure at night in Drosophila. 支链转氨酶活性降低可减轻果蝇夜间弱光暴露引起的代谢脆弱性。
IF 1.9 4区 医学 Q3 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-03-01 DOI: 10.1080/01677063.2022.2144292
Mari Kim, Gwang-Ic Son, Yun-Ho Cho, Gye-Hyeong Kim, Sung-Eun Yun, Young-Joon Kim, Jongkyeong Chung, Eunil Lee, Joong-Jean Park

The rhythmic pattern of biological processes controlled by light over 24 h is termed the circadian rhythm. Disturbance of circadian rhythm due to exposure to light at night (LAN) disrupts the sleep-wake cycle and can promote cardiovascular disease, diabetes, cancer, and metabolic disorders in humans. We studied how dim LAN affects the circadian rhythm and metabolism using male Drosophila. Wild-type flies exposed to the dim light of 10 lux at night displayed altered 24 h sleep-wake behavior and expression patterns of circadian rhythm genes. In addition, the flies became more vulnerable to metabolic stress, such as starvation. Whole-body metabolite analysis revealed decreased amounts of branched-chain amino acids (BCAAs), such as isoleucine and valine. The dim light exposure also increased the expression of branched-chain amino acid aminotransferase (BCAT) and branched-chain α-keto acid dehydrogenase (BCKDC) enzyme complexes that regulate the metabolism of BCAAs. Flies with the Bcat heterozygous mutation were not vulnerable to starvation stress, even when exposed to dim LAN, and hemolymph BCAA levels did not decrease in these flies. Furthermore, the vulnerability to starvation stress was also suppressed when the Bcat expression level was reduced in the whole body, neurons, or fat body during adulthood using conditional GAL4 and RNA interference. Finally, the metabolic vulnerability was reversed when BCAAs were fed to wild-type flies exposed to LAN. Thus, short-term dim light exposure at night affects the expression of circadian genes and BCAA metabolism in Drosophila, implying a novel function of BCAAs in suppressing metabolic stress caused by disrupted circadian rhythm.

光在24小时内控制生物过程的节律模式被称为昼夜节律。夜间光照引起的昼夜节律紊乱会扰乱睡眠-觉醒周期,并可能导致人类心血管疾病、糖尿病、癌症和代谢紊乱。我们以雄性果蝇为研究对象,研究了暗LAN对果蝇昼夜节律和代谢的影响。夜间暴露在10勒克斯的昏暗光线下的野生型果蝇表现出24小时睡眠-觉醒行为和昼夜节律基因表达模式的改变。此外,果蝇更容易受到代谢压力的影响,比如饥饿。全身代谢物分析显示支链氨基酸(BCAAs)的数量减少,如异亮氨酸和缬氨酸。昏暗光照还增加了调节BCAAs代谢的支链氨基酸转氨酶(BCAT)和支链α-酮酸脱氢酶(BCKDC)酶复合物的表达。携带Bcat杂合突变的果蝇不容易受到饥饿应激,即使暴露在昏暗的LAN中,这些果蝇的血淋巴BCAA水平也没有下降。此外,通过条件GAL4和RNA干扰,降低成年期全身、神经元或脂肪体的Bcat表达水平,也抑制了对饥饿应激的易损性。最后,当BCAAs被喂食给暴露于LAN的野生型果蝇时,代谢脆弱性被逆转。因此,夜间短时间的昏暗光照会影响果蝇昼夜节律基因的表达和BCAA代谢,这意味着BCAA具有抑制昼夜节律紊乱引起的代谢应激的新功能。
{"title":"Reduced branched-chain aminotransferase activity alleviates metabolic vulnerability caused by dim light exposure at night in <i>Drosophila</i>.","authors":"Mari Kim,&nbsp;Gwang-Ic Son,&nbsp;Yun-Ho Cho,&nbsp;Gye-Hyeong Kim,&nbsp;Sung-Eun Yun,&nbsp;Young-Joon Kim,&nbsp;Jongkyeong Chung,&nbsp;Eunil Lee,&nbsp;Joong-Jean Park","doi":"10.1080/01677063.2022.2144292","DOIUrl":"https://doi.org/10.1080/01677063.2022.2144292","url":null,"abstract":"<p><p>The rhythmic pattern of biological processes controlled by light over 24 h is termed the circadian rhythm. Disturbance of circadian rhythm due to exposure to light at night (LAN) disrupts the sleep-wake cycle and can promote cardiovascular disease, diabetes, cancer, and metabolic disorders in humans. We studied how dim LAN affects the circadian rhythm and metabolism using male <i>Drosophila</i>. Wild-type flies exposed to the dim light of 10 lux at night displayed altered 24 h sleep-wake behavior and expression patterns of circadian rhythm genes. In addition, the flies became more vulnerable to metabolic stress, such as starvation. Whole-body metabolite analysis revealed decreased amounts of branched-chain amino acids (BCAAs), such as isoleucine and valine. The dim light exposure also increased the expression of branched-chain amino acid aminotransferase (BCAT) and branched-chain α-keto acid dehydrogenase (BCKDC) enzyme complexes that regulate the metabolism of BCAAs. Flies with the <i>Bcat</i> heterozygous mutation were not vulnerable to starvation stress, even when exposed to dim LAN, and hemolymph BCAA levels did not decrease in these flies. Furthermore, the vulnerability to starvation stress was also suppressed when the <i>Bcat</i> expression level was reduced in the whole body, neurons, or fat body during adulthood using conditional GAL4 and RNA interference. Finally, the metabolic vulnerability was reversed when BCAAs were fed to wild-type flies exposed to LAN. Thus, short-term dim light exposure at night affects the expression of circadian genes and BCAA metabolism in <i>Drosophila</i>, implying a novel function of BCAAs in suppressing metabolic stress caused by disrupted circadian rhythm.</p>","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":null,"pages":null},"PeriodicalIF":1.9,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9785853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Knockdown of glutathione S-transferase leads to mislocalization and accumulation of cabeza, a drosophila homolog of FUS, in the brain. 谷胱甘肽s -转移酶的敲低导致cabeza在大脑中的错误定位和积累,cabeza是果蝇FUS的同源物。
IF 1.9 4区 医学 Q3 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-03-01 DOI: 10.1080/01677063.2022.2149747
Sun Joo Cha, Ja Hoon Yoon, Yeo Jeong Han, Kiyoung Kim

Glutathione S-transferase omega (GSTO) is an antioxidant enzyme involved in reducing oxidative stress. Recent studies suggest that polymorphic variants of GSTOs affect the onset age and progression of neurodegenerative diseases. Although GSTO activity may affect the development and age dependency of several diseases, the mechanism by which GSTO inactivation in neurons regulates the susceptibility to neurodegenerative diseases is unclear. In the present study, GstO2 knockdown in Drosophila led to increased levels of Cabeza (Caz) protein in neurons in an age-dependent manner. Drosophila Caz is the ortholog of human FUS, which is associated with neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). We found that cytoplasmic Caz mislocalization and aggregation in neurons significantly increased after GstO2 knockdown in vivo. Downregulation of GstO2 decreased the solubility of the Caz protein in aging neurons. These findings demonstrate that GSTO is a critical modulator of the development of neurodegenerative diseases by regulating Caz localization and aggregation in the nervous system of Drosophila.

谷胱甘肽s -转移酶(GSTO)是一种抗氧化酶,参与减少氧化应激。最近的研究表明,GSTOs的多态性变异影响神经退行性疾病的发病年龄和进展。虽然GSTO活性可能影响多种疾病的发展和年龄依赖性,但神经元中GSTO失活调控神经退行性疾病易感性的机制尚不清楚。在本研究中,果蝇中GstO2的敲低导致神经元中Cabeza (Caz)蛋白水平以年龄依赖的方式增加。Caz果蝇是人类FUS的同源基因,它与神经退行性疾病有关,包括肌萎缩侧索硬化症(ALS)和额颞叶痴呆(FTD)。我们发现GstO2敲除后神经元胞质Caz错定位和聚集显著增加。GstO2的下调降低了老化神经元中Caz蛋白的溶解度。这些发现表明GSTO通过调节果蝇神经系统中Caz的定位和聚集,是神经退行性疾病发展的重要调节剂。
{"title":"Knockdown of glutathione S-transferase leads to mislocalization and accumulation of cabeza, a <i>drosophila</i> homolog of FUS, in the brain.","authors":"Sun Joo Cha,&nbsp;Ja Hoon Yoon,&nbsp;Yeo Jeong Han,&nbsp;Kiyoung Kim","doi":"10.1080/01677063.2022.2149747","DOIUrl":"https://doi.org/10.1080/01677063.2022.2149747","url":null,"abstract":"<p><p>Glutathione S-transferase omega (GSTO) is an antioxidant enzyme involved in reducing oxidative stress. Recent studies suggest that polymorphic variants of GSTOs affect the onset age and progression of neurodegenerative diseases. Although GSTO activity may affect the development and age dependency of several diseases, the mechanism by which GSTO inactivation in neurons regulates the susceptibility to neurodegenerative diseases is unclear. In the present study, <i>GstO2</i> knockdown in <i>Drosophila</i> led to increased levels of Cabeza (Caz) protein in neurons in an age-dependent manner. <i>Drosophila</i> Caz is the ortholog of human FUS, which is associated with neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). We found that cytoplasmic Caz mislocalization and aggregation in neurons significantly increased after <i>GstO2</i> knockdown <i>in vivo</i>. Downregulation of <i>GstO2</i> decreased the solubility of the Caz protein in aging neurons. These findings demonstrate that GSTO is a critical modulator of the development of neurodegenerative diseases by regulating Caz localization and aggregation in the nervous system of <i>Drosophila</i>.</p>","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":null,"pages":null},"PeriodicalIF":1.9,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9788818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
History of Drosophila neurogenetic research in South Korea. 韩国果蝇神经遗传学研究的历史。
IF 1.9 4区 医学 Q3 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-03-01 DOI: 10.1080/01677063.2022.2115040
Greg S B Suh, Kweon Yu, Young-Joon Kim, Yangkyun Oh, Joong-Jean Park

Neurogenetic research using the Drosophila model has immensely expanded around the world. Likewise, scientists in South Korea have leveraged the advantages of Drosophila genetic tools to understand various neurobiological processes. In this special issue, we will overview the history of Drosophila neurogenetic research in South Korea that led to significant discoveries and notably implications. We will describe how Drosophila system was first introduced to elevate neural developmental studies in 1990s. Establishing Drosophila-related resources has been a key venture, which led to the generation of over 100,000 mutant lines and the launch of the K-Gut initiative with Korea Drosophila Research Center (KDRC). These resources have supported the pioneer studies in modeling human disease and understanding genes and neural circuits that regulate animal behavior and physiology.

使用果蝇模型的神经遗传学研究在世界范围内得到了极大的扩展。同样,韩国科学家利用果蝇遗传工具的优势来理解各种神经生物学过程。在本期特刊中,我们将概述韩国果蝇神经遗传学研究的历史,这些研究导致了重大发现和显著影响。我们将描述果蝇系统如何在20世纪90年代首次被引入以提升神经发育研究。建立与果蝇相关的资源是一项关键的冒险,它导致了超过10万个突变系的产生,并与韩国果蝇研究中心(KDRC)启动了K-Gut计划。这些资源支持了人类疾病建模和理解调节动物行为和生理的基因和神经回路的先驱研究。
{"title":"History of <i>Drosophila</i> neurogenetic research in South Korea.","authors":"Greg S B Suh,&nbsp;Kweon Yu,&nbsp;Young-Joon Kim,&nbsp;Yangkyun Oh,&nbsp;Joong-Jean Park","doi":"10.1080/01677063.2022.2115040","DOIUrl":"https://doi.org/10.1080/01677063.2022.2115040","url":null,"abstract":"<p><p>Neurogenetic research using the <i>Drosophila</i> model has immensely expanded around the world. Likewise, scientists in South Korea have leveraged the advantages of <i>Drosophila</i> genetic tools to understand various neurobiological processes. In this special issue, we will overview the history of <i>Drosophila</i> neurogenetic research in South Korea that led to significant discoveries and notably implications. We will describe how <i>Drosophila</i> system was first introduced to elevate neural developmental studies in 1990s. Establishing <i>Drosophila</i>-related resources has been a key venture, which led to the generation of over 100,000 mutant lines and the launch of the K-Gut initiative with Korea <i>Drosophila</i> Research Center (KDRC). These resources have supported the pioneer studies in modeling human disease and understanding genes and neural circuits that regulate animal behavior and physiology.</p>","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":null,"pages":null},"PeriodicalIF":1.9,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10187434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Editorial/preface: Neurogenetics innovation in South Korea. 社论/前言:韩国的神经遗传学创新。
IF 1.9 4区 医学 Q3 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-03-01 DOI: 10.1080/01677063.2023.2216054
Jing W Wang, Greg S B Suh, Chun-Fang Wu
Expanding the representation of research from countries beyond Europe and North America is a goal for the Journal of Neurogenetics. This special issue is designed to highlight the flourishing discipline of Drosophila neurogenetics in South Korea. The aim is to provide readers with a snapshot of the diverse research areas that are at the cutting edge of the field. Neurogenetics, the single-gene approach to study a wide range of neurobiological phenomena from the assembly of the nervous system, neurophysiology and circuit function to animal behaviors, has withstood early criticisms. Today, it stands as a fullyfledged and flourishing field. Early research efforts were focused on neural development and behavior, for which many genetic tools were produced. As these tools became more sophisticated, they were utilized to delve deeper and provide better mechanistic insights. The evolution of Drosophila neurogenetics in South Korea remarkably mirrors this progression. In the 1990s, a vast array of mutant lines was generated to study neural development, which enabled researchers to extend their investigations beyond their original questions. This expansion of research horizons fueled the creation of new and more advanced genetic reagents. This cycle of innovating with old tools, which eventually leads to the development of new ones, is a perfect encapsulation of the spirit of neurogenetics. This special issue is structured into four sections, beginning with the molecular mechanisms of neurodegeneration (Cha et al., 2022; Lee, Jo, et al., 2022), followed by the sensory modulation of sleep and arousal (Kim et al., 2022; Lee & Lim, 2022), then the use of machine learning to interrogate animal behaviors (Kim, An, et al., 2023; Kim, Kim, et al., 2023), and finally, nutrient sensors in feeding and non-feeding behaviors (Oh & Suh, 2022; Kim et al., 2023; Yoon et al., 2022). These studies offer exciting new findings as well as sketch out the future directions for the field in South Korea and around the world.
{"title":"Editorial/preface: Neurogenetics innovation in South Korea.","authors":"Jing W Wang,&nbsp;Greg S B Suh,&nbsp;Chun-Fang Wu","doi":"10.1080/01677063.2023.2216054","DOIUrl":"https://doi.org/10.1080/01677063.2023.2216054","url":null,"abstract":"Expanding the representation of research from countries beyond Europe and North America is a goal for the Journal of Neurogenetics. This special issue is designed to highlight the flourishing discipline of Drosophila neurogenetics in South Korea. The aim is to provide readers with a snapshot of the diverse research areas that are at the cutting edge of the field. Neurogenetics, the single-gene approach to study a wide range of neurobiological phenomena from the assembly of the nervous system, neurophysiology and circuit function to animal behaviors, has withstood early criticisms. Today, it stands as a fullyfledged and flourishing field. Early research efforts were focused on neural development and behavior, for which many genetic tools were produced. As these tools became more sophisticated, they were utilized to delve deeper and provide better mechanistic insights. The evolution of Drosophila neurogenetics in South Korea remarkably mirrors this progression. In the 1990s, a vast array of mutant lines was generated to study neural development, which enabled researchers to extend their investigations beyond their original questions. This expansion of research horizons fueled the creation of new and more advanced genetic reagents. This cycle of innovating with old tools, which eventually leads to the development of new ones, is a perfect encapsulation of the spirit of neurogenetics. This special issue is structured into four sections, beginning with the molecular mechanisms of neurodegeneration (Cha et al., 2022; Lee, Jo, et al., 2022), followed by the sensory modulation of sleep and arousal (Kim et al., 2022; Lee & Lim, 2022), then the use of machine learning to interrogate animal behaviors (Kim, An, et al., 2023; Kim, Kim, et al., 2023), and finally, nutrient sensors in feeding and non-feeding behaviors (Oh & Suh, 2022; Kim et al., 2023; Yoon et al., 2022). These studies offer exciting new findings as well as sketch out the future directions for the field in South Korea and around the world.","PeriodicalId":16491,"journal":{"name":"Journal of neurogenetics","volume":null,"pages":null},"PeriodicalIF":1.9,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10173262","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
期刊
Journal of neurogenetics
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1