Mutations of the Electron Transport Chain Affect Lifespan and ROS Levels in <i>C. elegans</i> by Fanni Ősz, Aamir Nazir, Krisztina Takács-Vellai, Zsolt Farkas

“…This review explores the structure and function of the ETC in the context of its role in mtROS generation and regulation, emphasizing its dual roles in cellular damage and signaling. Using <i>Caenorhabditis elegans</i> as a model organism, we discuss how ETC mutations manifest as developmental abnormalities, lifespan alterations, and changes in mtROS levels. …”
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Tau phosphorylation suppresses oxidative stress-induced mitophagy via FKBP8 receptor modulation. by Michael O Isei, Meredith Crockett, Emily Chen, Joel Rodwell-Bullock, Trae Carroll, Peter A Girardi, Keith Nehrke, Gail V W Johnson

“…Previously, we showed that tau which has been mutated at Thr-231 to glutamic acid to mimic an Alzheimer's-relevant phospho-epitope expressed early in disease selectively inhibits oxidative stress-induced mitophagy in Caenorhabditis elegans. Here, we use immortalized mouse hippocampal neuronal cell lines to extend that result into mammalian cells. …”
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Spherical harmonics texture extraction for versatile analysis of biological objects. by Oane Gros, Josiah B Passmore, Noa O Borst, Dominik Kutra, Wilco Nijenhuis, Timothy Fuqua, Lukas C Kapitein, Justin M Crocker, Anna Kreshuk, Simone Köhler

“…Our method can also quantify morphological differences in Caenorhabditis elegans germline nuclei, which lack a predefined pattern. …”
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Intergenerational transport of double-stranded RNA in C. elegans can limit heritable epigenetic changes by Nathan M Shugarts Devanapally, Aishwarya Sathya, Andrew L Yi, Winnie M Chan, Julia A Marre, Antony M Jose

“…Such RNA can cross generational boundaries, as evidenced by somatic double-stranded RNA (dsRNA) in the nematode Caenorhabditis elegans silencing genes of matching sequence in progeny. …”
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Geroprotection from ergothioneine treatment in Drosophila melanogaster by improving intestinal barrier and activation of intestinal autophagy by Hongyu Pan, Qianwang Zheng, Yuan Zou, Guozhao Luo, Mingzhen Tu, Na Wang, Jingru Zhong, Liqiong Guo, Junfang Lin

“…Previous studies have demonstrated that ergothioneine can increase the lifespan of Drosophila melanogaster and Caenorhabditis elegans, and enhance telomerase activity. In present study, the metagenomics sequencing and quantitative real-time polymerase chain reaction analysis were employed to characterize the composition and diversity of gut microbiome in aging flies. …”
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Unravelling anti-cancer properties of solanaceous extracts using GC–MS and HPLC by Iqra Riaz, Yamin Bibi, Muhammad Arshad, Muhammad Sheeraz Ahmad, Manzer H. Siddiqui, Yawen Zeng, Abdul Qayyum

“…Brine shrimps, cell lines (A549, Hela, HEPG), and Caenorhabditis elegans were used initially to examine three solanaceous plant extracts (Solanum villosum (SV), Cestrum aurantiacum (CA), and Brugmansia suaveolens (BS)). …”
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Multispanning membrane protein SIDT2 increases knockdown activity of gapmer antisense oligonucleotides by Kohshi Kusumoto, Kiyomi Sasaki, Yasunori Uchida, Ayaka Utsumi, Tokuyuki Yoshida, Satoshi Obika, Takao Inoue, Keiichiro Okuhira

“…In the nematode, Caenorhabditis elegans, the multi-pass transmembrane protein, SID-1, is involved in the cellular uptake of double-stranded RNAs. …”
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Functional analysis of conserved C. elegans bHLH family members uncovers lifespan control by a peptidergic hub neuron. by G Robert Aguilar, Berta Vidal, Hongzhu Ji, Joke Evenblij, Chien-Po Liao, Hongfei Ji, Giulio Valperga, Christopher Fang-Yen, Oliver Hobert

“…We analyze here the function of 5 Caenorhabditis elegans bHLH genes, falling into 3 phylogenetically conserved subfamilies, which are continuously expressed in a very small number of postmitotic neurons in the central nervous system. …”
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A distant TANGO1 family member promotes vitellogenin export from the ER in C. elegans by Jimmy H. Mo, Chao Zhai, Kwangsek Jung, Yan Li, Yonghong Yan, Meng-Qiu Dong, Ho Yi Mak

“…Summary: Vitellogenin is thought to share a common ancestor with human apolipoprotein B (ApoB) for systemic lipid transport. In Caenorhabditis elegans, although a general route for inter-tissue vitellogenin transport has been described, the full mechanism that underlies its intracellular trafficking within the intestine remains obscure. …”
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Increased RTN3 phenocopies nonalcoholic fatty liver disease by inhibiting the AMPK–IDH2 pathway by Hao Huang, Shuai Guo, Ya‐Qin Chen, Yu‐Xing Liu, Jie‐Yuan Jin, Yun Liang, Liang‐Liang Fan, Rong Xiang

“…We further showed this in primary hepatocytes, the L02 cell line, and the Caenorhabditis elegans strain. Mechanistically, RTN3 regulated these events through its interactions with glucose‐regulated protein 78 (GRP78), which further inhibited the adenosine 5 monophosphate‐activated protein kinase (AMPK)–isocitrate dehydrogenase 2 (IDH2) pathway. …”
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DDX3 participates in miRNA biogenesis and RNA interference through translational control of PACT and interaction with AGO2 by Ming‐Chih Lai, Yen‐Ling Yu, Chiao‐Nung Chen, Jau‐Song Yu, Hsin‐Yuan Hung, Shih‐Peng Chan

“…Here, we showed that the control of PACT by DDX3 is conserved in human cells and Caenorhabditis elegans. Using a miRNA microarray, we found that DDX3 regulates the expression of a small subset of cancer‐related miRNAs. …”
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Non-cell-autonomous regulation of mTORC2 by Hedgehog signaling maintains lipid homeostasis by Kylie R. VanDerMolen, Martin A. Newman, Peter C. Breen, Yunjing Gao, Laura A. Huff, Robert H. Dowen

“…Here, we identify a non-canonical role for Hedgehog (Hh), a classic regulator of development, in maintaining intestinal lipid homeostasis in Caenorhabditis elegans. We demonstrate, using C. elegans and mouse hepatocytes, that Hh metabolic regulation does not occur through the canonical Hh transcription factor TRA-1/GLI, but rather via non-canonical signaling that engages mammalian target of rapamycin complex 2 (mTORC2). …”
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Gene regulatory patterning codes in early cell fate specification of the C. elegans embryo by Alison G Cole, Tamar Hashimshony, Zhuo Du, Itai Yanai

“…This classic model however does not translate directly to species that lack a syncytium – such as Caenorhabditis elegans – where cell fate is specified by cell-autonomous cell lineage programs and their inter-signaling. …”
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OSP-1 protects neurons from autophagic cell death induced by acute oxidative stress by Alessandra Donato, Fiona K. Ritchie, Lachlan Lu, Mehershad Wadia, Ramon Martinez-Marmol, Eva Kaulich, Kornraviya Sankorrakul, Hang Lu, Sean Coakley, Elizabeth J. Coulson, Massimo A. Hilliard

“…However, our knowledge of the genetic elements that can be manipulated to protect neurons from oxidative stress-induced cell death is still very limited. Here, using Caenorhabditis elegans as a model system, combined with the optogenetic tool KillerRed to spatially and temporally control ROS generation, we identify a previously uncharacterized gene, oxidative stress protective 1 (osp-1), that protects C. elegans neurons from oxidative damage. …”
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Therapeutic Potential of <i>Lappula patula</i> Extracts on Germline Development and DNA Damage Responses in <i>C. elegans</i> by Qinghao Meng, Anna Hu, Weiyu Xiao, Robert P. Borris, Hyun-Min Kim

“…This study aimed to evaluate the nematocidal effects of L. patula extracts and investigate their impact on germline development, DNA damage responses, and apoptosis in <i>Caenorhabditis elegans (C. elegans</i>), a model organism for studying these processes. …”
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Animal models in biomedical research: Relevance of Drosophila melanogaster by Olabisi Tajudeen Obafemi, Ademola Olabode Ayeleso, Olusola Bolaji Adewale, Jeremiah Unuofin, Bidemi Emmanuel Ekundayo, Monde Ntwasa, Sogolo Lucky Lebelo

“…These models could range in complexity from Caenorhabditis elegans to non-human primates. With the aid of these animal models, a lot of new knowledge has been gained about several diseases which otherwise would not have been possible. …”
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Alzheimer-mutant γ-secretase complexes stall amyloid β-peptide production by Parnian Arafi, Sujan Devkota, Emily Williams, Masato Maesako, Michael S Wolfe

“…These stalled complexes triggered synaptic degeneration in a Caenorhabditis elegans model of FAD independently of Aβ production. …”
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A microbiota-derived metabolite, 3-phenyllactic acid, prolongs healthspan by enhancing mitochondrial function and stress resilience via SKN-1/ATFS-1 in C. elegans by Juewon Kim, Yunju Jo, Gyumin Lim, Yosep Ji, Jong-Hwa Roh, Wan-Gi Kim, Hyon-Seung Yi, Dong Wook Choi, Donghyun Cho, Dongryeol Ryu

“…While previous studies primarily focus on the discovery of novel bioactive bacteria and alterations in the microbiome environment to explain potential probiotic effects, our research delves into the role of living Lactiplantibacillus (formerly known as Lactobacillus) and their conditioned media, highlighting that only the former, not dead bacteria, enhance the healthspan of Caenorhabditis elegans (C. elegans). To elucidate the underlying mechanisms, we conduct transcriptomic profiling through RNA-seq analysis in C. elegans exposed to GTB1, a strain of Lactiplantibacillus plantarum or 3-phenyllactic acid (PLA), mimicking the presence of key candidate metabolites of GTB1 and evaluating healthspan. …”
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Naturally occurring variation in a cytochrome P450 modifies thiabendazole responses independently of beta-tubulin. by J B Collins, Clayton M Dilks, Steffen R Hahnel, Briana Rodriguez, Bennett W Fox, Elizabeth Redman, Jingfang Yu, Brittany Cooke, Kateryna Sihuta, Mostafa Zamanian, Peter J Roy, Frank C Schroeder, John S Gilleard, Erik C Andersen

“…We performed a genome-wide association study using a genetically diverse panel of Caenorhabditis elegans strains to identify loci that contribute to resistance to the BZ drug thiabendazole (TBZ). …”
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Decreased SynMuv B gene activity in response to viral infection leads to activation of the antiviral RNAi pathway in C. elegans. by Ashwin Seetharaman, Himani Galagali, Elizabeth Linarte, Mona H X Liu, Jennifer D Cohen, Kashish Chetal, Ruslan Sadreyev, Alex J Tate, Taiowa A Montgomery, Gary Ruvkun

“…RNA interference (RNAi) mediates antiviral defense in many eukaryotes. Caenorhabditis elegans mutants that disable RNAi are more sensitive to viral infection. …”
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