Protein & Cell最新文献

{"title":"The best practice for microbiome analysis using R.","authors":"Tao Wen,&nbsp;Guoqing Niu,&nbsp;Tong Chen,&nbsp;Qirong Shen,&nbsp;Jun Yuan,&nbsp;Yong-Xin Liu","doi":"10.1093/procel/pwad024","DOIUrl":"10.1093/procel/pwad024","url":null,"abstract":"<p><p>With the gradual maturity of sequencing technology, many microbiome studies have published, driving the emergence and advance of related analysis tools. R language is the widely used platform for microbiome data analysis for powerful functions. However, tens of thousands of R packages and numerous similar analysis tools have brought major challenges for many researchers to explore microbiome data. How to choose suitable, efficient, convenient, and easy-to-learn tools from the numerous R packages has become a problem for many microbiome researchers. We have organized 324 common R packages for microbiome analysis and classified them according to application categories (diversity, difference, biomarker, correlation and network, functional prediction, and others), which could help researchers quickly find relevant R packages for microbiome analysis. Furthermore, we systematically sorted the integrated R packages (phyloseq, microbiome, MicrobiomeAnalystR, Animalcules, microeco, and amplicon) for microbiome analysis, and summarized the advantages and limitations, which will help researchers choose the appropriate tools. Finally, we thoroughly reviewed the R packages for microbiome analysis, summarized most of the common analysis content in the microbiome, and formed the most suitable pipeline for microbiome analysis. This paper is accompanied by hundreds of examples with 10,000 lines codes in GitHub, which can help beginners to learn, also help analysts compare and test different tools. This paper systematically sorts the application of R in microbiome, providing an important theoretical basis and practical reference for the development of better microbiome tools in the future. All the code is available at GitHub github.com/taowenmicro/EasyMicrobiomeR.</p>","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":null,"pages":null},"PeriodicalIF":21.1,"publicationDate":"2023-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10599642/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9451539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The microbiota-gut-brain axis and neurodevelopmental disorders.","authors":"Qinwen Wang,&nbsp;Qianyue Yang,&nbsp;Xingyin Liu","doi":"10.1093/procel/pwad026","DOIUrl":"10.1093/procel/pwad026","url":null,"abstract":"<p><p>The gut microbiota has been found to interact with the brain through the microbiota-gut-brain axis, regulating various physiological processes. In recent years, the impacts of the gut microbiota on neurodevelopment through this axis have been increasingly appreciated. The gut microbiota is commonly considered to regulate neurodevelopment through three pathways, the immune pathway, the neuronal pathway, and the endocrine/systemic pathway, with overlaps and crosstalks in between. Accumulating studies have identified the role of the microbiota-gut-brain axis in neurodevelopmental disorders including autism spectrum disorder, attention deficit hyperactivity disorder, and Rett Syndrome. Numerous researchers have examined the physiological and pathophysiological mechanisms influenced by the gut microbiota in neurodevelopmental disorders (NDDs). This review aims to provide a comprehensive overview of advancements in research pertaining to the microbiota-gut-brain axis in NDDs. Furthermore, we analyzed both the current state of research progress and discuss future perspectives in this field.</p>","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":null,"pages":null},"PeriodicalIF":21.1,"publicationDate":"2023-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10599644/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9436908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microbiome research outlook: past, present, and future.","authors":"Yunyun Gao,&nbsp;Danyi Li,&nbsp;Yong-Xin Liu","doi":"10.1093/procel/pwad031","DOIUrl":"10.1093/procel/pwad031","url":null,"abstract":"With its critical role in human health and disease, the microbiome has transformed modern biology. Over the past few years, microbiome research has evolved rapidly, with microbiologists gradually shifting their focus from cataloging microorganisms in the human microbiome to understanding their functional roles and how they interact with the host. Here, we present the global trends in microbiome research and summarize the past and current work on microbiome published in Protein & Cell. In closing, we highlight some of the major advancements in microbiome research, including technical, practical, and conceptual advancements, that aim to enhance disease diagnosis, medicine development, and personalized interventions.","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":null,"pages":null},"PeriodicalIF":21.1,"publicationDate":"2023-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10599639/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9558360","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"\"Sentinel or accomplice\": gut microbiota and microglia crosstalk in disorders of gut-brain interaction.","authors":"Haonan Zheng,&nbsp;Cunzheng Zhang,&nbsp;Jindong Zhang,&nbsp;Liping Duan","doi":"10.1093/procel/pwad020","DOIUrl":"10.1093/procel/pwad020","url":null,"abstract":"<p><p>Abnormal brain-gut interaction is considered the core pathological mechanism behind the disorders of gut-brain interaction (DGBI), in which the intestinal microbiota plays an important role. Microglia are the \"sentinels\" of the central nervous system (CNS), which participate in tissue damage caused by traumatic brain injury, resist central infection and participate in neurogenesis, and are involved in the occurrence of various neurological diseases. With in-depth research on DGBI, we could find an interaction between the intestinal microbiota and microglia and that they are jointly involved in the occurrence of DGBI, especially in individuals with comorbidities of mental disorders, such as irritable bowel syndrome (IBS). This bidirectional regulation of microbiota and microglia provides a new direction for the treatment of DGBI. In this review, we focus on the role and underlying mechanism of the interaction between gut microbiota and microglia in DGBI, especially IBS, and the corresponding clinical application prospects and highlight its potential to treat DGBI in individuals with psychiatric comorbidities.</p>","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":null,"pages":null},"PeriodicalIF":21.1,"publicationDate":"2023-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10599645/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9384588","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of the microbiome on mosquito-borne diseases.","authors":"Huicheng Shi,&nbsp;Xi Yu,&nbsp;Gong Cheng","doi":"10.1093/procel/pwad021","DOIUrl":"10.1093/procel/pwad021","url":null,"abstract":"<p><p>Mosquito-borne diseases present a significant threat to human health, with the possibility of outbreaks of new mosquito-borne diseases always looming. Unfortunately, current measures to combat these diseases such as vaccines and drugs are often either unavailable or ineffective. However, recent studies on microbiomes may reveal promising strategies to fight these diseases. In this review, we examine recent advances in our understanding of the effects of both the mosquito and vertebrate microbiomes on mosquito-borne diseases. We argue that the mosquito microbiome can have direct and indirect impacts on the transmission of these diseases, with mosquito symbiotic microorganisms, particularly Wolbachia bacteria, showing potential for controlling mosquito-borne diseases. Moreover, the skin microbiome of vertebrates plays a significant role in mosquito preferences, while the gut microbiome has an impact on the progression of mosquito-borne diseases in humans. As researchers continue to explore the role of microbiomes in mosquito-borne diseases, we highlight some promising future directions for this field. Ultimately, a better understanding of the interplay between mosquitoes, their hosts, pathogens, and the microbiomes of mosquitoes and hosts may hold the key to preventing and controlling mosquito-borne diseases.</p>","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":null,"pages":null},"PeriodicalIF":21.1,"publicationDate":"2023-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10599646/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9469207","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunogenic molecules associated with gut bacterial cell walls: chemical structures, immune-modulating functions, and mechanisms.","authors":"Ruopeng Yin,&nbsp;Tao Wang,&nbsp;Huanqin Dai,&nbsp;Junjie Han,&nbsp;Jingzu Sun,&nbsp;Ningning Liu,&nbsp;Wang Dong,&nbsp;Jin Zhong,&nbsp;Hongwei Liu","doi":"10.1093/procel/pwad016","DOIUrl":"10.1093/procel/pwad016","url":null,"abstract":"<p><p>Interactions between gut microbiome and host immune system are fundamental to maintaining the intestinal mucosal barrier and homeostasis. At the host-gut microbiome interface, cell wall-derived molecules from gut commensal bacteria have been reported to play a pivotal role in training and remodeling host immune responses. In this article, we review gut bacterial cell wall-derived molecules with characterized chemical structures, including peptidoglycan and lipid-related molecules that impact host health and disease processes via regulating innate and adaptive immunity. Also, we aim to discuss the structures, immune responses, and underlying mechanisms of these immunogenic molecules. Based on current advances, we propose cell wall-derived components as important sources of medicinal agents for the treatment of infection and immune diseases.</p>","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":null,"pages":null},"PeriodicalIF":21.1,"publicationDate":"2023-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10599643/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9612156","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"METTL14 is a chromatin regulator independent of its RNA N6-methyladenosine methyltransferase activity.","authors":"Xiaoyang Dou, Lulu Huang, Yu Xiao, Chang Liu, Yini Li, Xinning Zhang, Lishan Yu, Ran Zhao, Lei Yang, Chuan Chen, Xianbin Yu, Boyang Gao, Meijie Qi, Yawei Gao, Bin Shen, Shuying Sun, Chuan He, Jun Liu","doi":"10.1093/procel/pwad009","DOIUrl":"10.1093/procel/pwad009","url":null,"abstract":"<p><p>METTL3 and METTL14 are two components that form the core heterodimer of the main RNA m6A methyltransferase complex (MTC) that installs m6A. Surprisingly, depletion of METTL3 or METTL14 displayed distinct effects on stemness maintenance of mouse embryonic stem cell (mESC). While comparable global hypo-methylation in RNA m6A was observed in Mettl3 or Mettl14 knockout mESCs, respectively. Mettl14 knockout led to a globally decreased nascent RNA synthesis, whereas Mettl3 depletion resulted in transcription upregulation, suggesting that METTL14 might possess an m6A-independent role in gene regulation. We found that METTL14 colocalizes with the repressive H3K27me3 modification. Mechanistically, METTL14, but not METTL3, binds H3K27me3 and recruits KDM6B to induce H3K27me3 demethylation independent of METTL3. Depletion of METTL14 thus led to a global increase in H3K27me3 level along with a global gene suppression. The effects of METTL14 on regulation of H3K27me3 is essential for the transition from self-renewal to differentiation of mESCs. This work reveals a regulatory mechanism on heterochromatin by METTL14 in a manner distinct from METTL3 and independently of m6A, and critically impacts transcriptional regulation, stemness maintenance, and differentiation of mESCs.</p>","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":null,"pages":null},"PeriodicalIF":21.1,"publicationDate":"2023-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10501186/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10312616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structural basis of INTAC-regulated transcription.","authors":"Hai Zheng,&nbsp;Qianwei Jin,&nbsp;Xinxin Wang,&nbsp;Yilun Qi,&nbsp;Weida Liu,&nbsp;Yulei Ren,&nbsp;Dan Zhao,&nbsp;Fei Xavier Chen,&nbsp;Jingdong Cheng,&nbsp;Xizi Chen,&nbsp;Yanhui Xu","doi":"10.1093/procel/pwad010","DOIUrl":"10.1093/procel/pwad010","url":null,"abstract":"1Fudan University Shanghai Cancer Center, Institutes of Biomedical Sciences, State Key Laboratory of Genetic Engineering, Shanghai Key Laboratory of Radiation Oncology, and Shanghai Key Laboratory of Medical Epigenetics, Shanghai Medical College of Fudan University, Shanghai 200032, China 2The International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, China, Department of Systems Biology for Medicine, School of Basic Medical Sciences, Shanghai Medical College of Fudan University, Shanghai 200032, China 3Human Phenome Institute, Collaborative Innovation Center of Genetics and Development, School of Life Sciences, Fudan University, Shanghai 200433, China ‡These authors contributed equally to this work. *Correspondence: zhengh@fudan.edu.cn (H. Zheng), xuyh@fudan.edu.cn (Y. Xu)","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":null,"pages":null},"PeriodicalIF":21.1,"publicationDate":"2023-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10501182/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10622466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Join the club: ORP8 is a lipophagy receptor.","authors":"Zheng Wang,&nbsp;Hong Zhang","doi":"10.1093/procel/pwad005","DOIUrl":"10.1093/procel/pwad005","url":null,"abstract":"Autophagy involves engulfment of cytosolic constituents in a de novo-synthesized double-membrane autophagosome and its subsequent delivery to the lysosome for degradation and recycling of sequestrated materials (Nakatogawa, 2020; Zhao et al., 2021). In terms of the cargo enclosed by the autophagosome, autophagy can be nonselective, in which a portion of the cytosol is indiscriminately sequestered; or highly selective, in which specific cargoes such as protein aggregates, superfluous/damaged organelles, or invading pathogens are engulfed (Vargas et al., 2022). Selective autophagy can be classified into different types according to the cargo, such as aggrephagy (protein aggregates), ER-phagy (endoplasmic reticulum), mitophagy (mitochondria) and lysophagy (lysosomes) (Vargas et al., 2022). During selective autophagy, a family of receptor proteins render the cargo capable of engaging with the autophagosomal precursor, called the isolation membrane (IM), with tight juxtaposition (Sawa-Makarska et al., 2014). The receptor recognizes cargoes via direct interaction, or indirectly such as via binding to a tag (e.g., polyubiquitin chains) added onto the cargo (Vargas et al., 2022). The receptor also interacts with LC3/GABARAP family autophagy proteins, which are conjugated to phosphatidylethanolamine on the IM (Johansen et al., 2020). The receptor can also recruit upstream autophagy proteins to initiate the formation of IMs surrounding cargoes (Vargas et al., 2022). Distinct receptors are utilized for degrading different cargoes. For example, p62, NBR1, TAXIBP1 and SEPA-1 mediate degradation of different protein cargoes; FAM134B, SEC62 and TEX264 act in ER-phagy; while FUNDC1, NDP52 and OPTN function in mitophagy (Chino and Mizushima, 2023; Vargas et al., 2022). Extensive studies have shown that the lipid droplet (LD), an organelle filled with neutral lipids such as triglycerides (TGs) and surrounded by a phospholipid monolayer, can be selectively degraded by autophagy, a process known as lipophagy. The receptor mediating this process, however, remains elusive. The gap is now filled by a study from the Liu lab published in this issue, showing that ORP8, a member of the oxysterol binding protein (OSBP) family, acts as a receptor to mediate lipophagy (Fig. 1) (Pu et al., 2022). LD biogenesis and turnover are tightly controlled to maintain lipid and energy homeostasis in cells (Zechner et al., 2017). To uncover potential receptors mediating lipophagy, Pu et al. performed mass spectrometry analysis to identify LC3associated LD proteins. LDs purified from cells treated with oleic acid (OA) (to stimulate LD biogenesis) and chloroquine (CQ) (to block lysosomal degradation) were lysed and affinity-precipitated by GST-LC3B. ORP8 was identified from the precipitates. ORP8, but not other OSBP family members such as OSBP, ORP2 and ORP5, interacted with LC3 upon lipophagy induction. ORP8 is an ER-resident lipid transporter protein mediating the counter-transport of pho","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":null,"pages":null},"PeriodicalIF":21.1,"publicationDate":"2023-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10501181/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10604740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ORP8 acts as a lipophagy receptor to mediate lipid droplet turnover.","authors":"Maomao Pu,&nbsp;Wenhui Zheng,&nbsp;Hongtao Zhang,&nbsp;Wei Wan,&nbsp;Chao Peng,&nbsp;Xuebo Chen,&nbsp;Xinchang Liu,&nbsp;Zizhen Xu,&nbsp;Tianhua Zhou,&nbsp;Qiming Sun,&nbsp;Dante Neculai,&nbsp;Wei Liu","doi":"10.1093/procel/pwac063","DOIUrl":"10.1093/procel/pwac063","url":null,"abstract":"<p><p>Lipophagy, the selective engulfment of lipid droplets (LDs) by autophagosomes for lysosomal degradation, is critical to lipid and energy homeostasis. Here we show that the lipid transfer protein ORP8 is located on LDs and mediates the encapsulation of LDs by autophagosomal membranes. This function of ORP8 is independent of its lipid transporter activity and is achieved through direct interaction with phagophore-anchored LC3/GABARAPs. Upon lipophagy induction, ORP8 has increased localization on LDs and is phosphorylated by AMPK, thereby enhancing its affinity for LC3/GABARAPs. Deletion of ORP8 or interruption of ORP8-LC3/GABARAP interaction results in accumulation of LDs and increased intracellular triglyceride. Overexpression of ORP8 alleviates LD and triglyceride deposition in the liver of ob/ob mice, and Osbpl8-/- mice exhibit liver lipid clearance defects. Our results suggest that ORP8 is a lipophagy receptor that plays a key role in cellular lipid metabolism.</p>","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":null,"pages":null},"PeriodicalIF":21.1,"publicationDate":"2023-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10501187/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10316509","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}