microPublication biologyPub Date : 2025-08-01eCollection Date: 2025-01-01DOI: 10.17912/micropub.biology.001497
Matthew Hull, Joslyn Mills
{"title":"<i>cnnm-5</i> knockdown improves proteostasis of mutant Huntingtin protein in <i>C. elegans</i>.","authors":"Matthew Hull, Joslyn Mills","doi":"10.17912/micropub.biology.001497","DOIUrl":"10.17912/micropub.biology.001497","url":null,"abstract":"<p><p>Huntington's disease (HD) is an age-related neurodegenerative disease associated with the aggregation of mutant Huntingtin protein (mHTT). It is theorized that prevention or clearance of these aggregates through autophagy and the ubiquitin proteasome system (UPS) protects neurons from degeneration. Using a <i>C. elegans</i> model of HD, a small reverse genetic screen of 100 random genes on Chromosome 3 identified <i>cnnm-5</i> as a genetic modifier of mHTT accumulation. During development, loss of <i>cnnm-5</i> by RNAi ( <i>cnnm-5</i> i) protects against mHTT accumulation, implicating <i>cnnm-5</i> as a negative regulator of protein aggregation prevention or clearance. Here we report that knocking down <i>cnnm-5</i> leads to decreased mHTT protein aggregation through the upregulation of the UPS and autophagy pathways, leading to increased lifespan. Further experimentation using a nematode model of Alzheimer's disease demonstrates <i>cnnm-5</i> i protects against paralysis by decreasing beta amyloid protein misfolding in body wall muscles.</p>","PeriodicalId":74192,"journal":{"name":"microPublication biology","volume":"2025 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12358017/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144877121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
microPublication biologyPub Date : 2025-07-31eCollection Date: 2025-01-01DOI: 10.17912/micropub.biology.001667
Joshua C Hincks, Jade G Stair, Nicole F Liachko
{"title":"Expression of polyglutamine repeats at the pathogenic threshold modestly enhances tau neurotoxicity and protein accumulation in <i>C. elegans</i>.","authors":"Joshua C Hincks, Jade G Stair, Nicole F Liachko","doi":"10.17912/micropub.biology.001667","DOIUrl":"10.17912/micropub.biology.001667","url":null,"abstract":"<p><p>CAG repeat expansions within the HTT gene cause Huntington's disease (HD), a devastating neurodegenerative disease characterized by progressive movement, cognitive, and behavioral symptoms. These expansions result in the expression and accumulation of neurotoxic poly-glutamine (polyQ). Disease initiation depends on the length of the expansion, with fewer than 35 repeats of polyQ typically not pathogenic, while 40 or greater repeats almost always result in HD. Longer expansions correlate with earlier onset of disease; however, there may be other factors that contribute to disease initiation or progression, particularly in individuals with repeat lengths close to or below the 40 repeat length pathogenic threshold. Aggregates of the protein tau are a frequent co-pathology in HD and may modify disease presentation. To examine relationships between tau and polyQ <i>in vivo</i> , we generated <i>C. elegans</i> co-expressing 40 repeats of polyQ (polyQ(40)) and human tau pan-neuronally. We found that co-expression of tau and polyQ(40) results in mild worsening of motility defects and increased accumulation of total and phosphorylated tau but not polyQ. These results suggest that co-morbid tau and polyQ can worsen neuronal dysfunction, and the presence of tau pathology may contribute to disease phenotypes in patients with HD, particularly individuals with repeat lengths close to the pathogenic threshold.</p>","PeriodicalId":74192,"journal":{"name":"microPublication biology","volume":"2025 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12364516/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144981606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Allopurinol treatment changes microglial characteristics in neonatal mice.","authors":"Rin-Ichiro Teruya, Tomomi Okajima-Takahashi, Fuminori Tsuruta","doi":"10.17912/micropub.biology.001739","DOIUrl":"10.17912/micropub.biology.001739","url":null,"abstract":"<p><p>Microglia are resident immune cells that play crucial roles in regulating brain development. During the pre and postnatal stage, microglial morphology gradually alters by the elongation of processes and an increase in the number of branches. Previously, we reported that hypoxanthine, a key intermediate of the purine metabolism, affects the morphology of microglial cell line BV2. In this study, we show that administration of allopurinol, an inhibitor of xanthine oxidase, changes microglial morphology <i>in vivo</i> . We found that the number of branches and summed length of processes are increased in allopurinol-treated microglia in a sex-independent manner. Notably, allopurinol administration altered the number of IBA1-positive microglia in male mice. These findings suggest that purine metabolism contributes to the regulation of microglial characteristics during neonatal brain development.</p>","PeriodicalId":74192,"journal":{"name":"microPublication biology","volume":"2025 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12364548/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144981470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
microPublication biologyPub Date : 2025-07-30eCollection Date: 2025-01-01DOI: 10.17912/micropub.biology.001638
Kayla M Komondor, Katherine G Sharp, Anne E Carlson
{"title":"Fertilization in the African clawed frog <i>, Xenopus laevis</i> , requires an egg-derived PLC to signal the fast block to polyspermy.","authors":"Kayla M Komondor, Katherine G Sharp, Anne E Carlson","doi":"10.17912/micropub.biology.001638","DOIUrl":"10.17912/micropub.biology.001638","url":null,"abstract":"<p><p>Fertilization in <i>Xenopus laevis</i> triggers calcium release and membrane depolarization to activate the fast block to polyspermy. This depolarization requires phospholipase C (PLC) activity, but the identity and origin of the PLC remained unclear. We previously reported that <i>PLCZ1</i> , which encodes the sperm-derived PLCζ used in mammals and birds, was deleted in Pipidae frogs, suggesting an alternative mechanism. Here, we used the irreversible PLC inhibitor U73122 to test whether the PLC driving the fast block originates from the egg or sperm. Inhibiting PLC activity in the egg, but not in the sperm, abolished the fertilization-evoked depolarization and led to polyspermy. These findings demonstrate that <i>X. laevis</i> relies on an egg-derived PLC to signal the fast block, revealing a fertilization-triggered calcium signaling pathway that is mechanistically distinct from other vertebrates.</p>","PeriodicalId":74192,"journal":{"name":"microPublication biology","volume":"2025 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12364549/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144981547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
microPublication biologyPub Date : 2025-07-30eCollection Date: 2025-01-01DOI: 10.17912/micropub.biology.001706
Amanda Dimatteo, Nicole Stango, Adam Rich, Tara Sweet
{"title":"Evaluating the molecular function of zebrafish Anoctamin 1a.","authors":"Amanda Dimatteo, Nicole Stango, Adam Rich, Tara Sweet","doi":"10.17912/micropub.biology.001706","DOIUrl":"10.17912/micropub.biology.001706","url":null,"abstract":"<p><p>Calcium-activated chloride channels (CaCCs) regulate key physiological processes like epithelial secretion, sensory transduction, gastrointestinal pacemaking, and muscle contraction. Zebrafish ( <i>Danio rerio</i> ) are genetically similar to humans, easily manipulated, and are a valuable model organism. We cloned zebrafish Anoctamin 1, a putative CaCC gene, expressed it in mammalian cells, and confirmed its function via halide flux assays. The channel conducted anions and responded to calcium, verifying its role as a CaCC. These findings confirm the functionality of zebrafish CaCCs and lay the groundwork to use the organism to model human physiology and disease.</p>","PeriodicalId":74192,"journal":{"name":"microPublication biology","volume":"2025 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12364550/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144981617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
microPublication biologyPub Date : 2025-07-29eCollection Date: 2025-01-01DOI: 10.17912/micropub.biology.001678
Runa Sakamoto, Ibuki Y Takahashi, Koji Kato, Yoshiki Nakajima, Jian-Ren Shen, Ryo Nagao
{"title":"Purification and pigment analysis of diadinoxanthin-binding PSI-LHCI supercomplexes from <i>Euglena gracilis</i> strain Z.","authors":"Runa Sakamoto, Ibuki Y Takahashi, Koji Kato, Yoshiki Nakajima, Jian-Ren Shen, Ryo Nagao","doi":"10.17912/micropub.biology.001678","DOIUrl":"10.17912/micropub.biology.001678","url":null,"abstract":"<p><p><i>Euglena gracilis</i> exhibits a unique pigment profile distinct from land plants and green algae. In this study, we purified photosystem I supercomplexes containing light-harvesting complexes (PSI-LHCI) from <i>E. gracilis</i> strain Z and analyzed their biochemical and spectroscopic properties. The PSI-LHCI contained diadinoxanthin while lacking lutein and violaxanthin, which are characteristic of green-lineage organisms. The absorption and 77-K fluorescence spectra of <i>Euglena</i> PSI-LHCI showed the Qy peak of chlorophyll <i>a</i> at 675 nm and emission at 732 nm, respectively, comparable to land plant PSI-LHCI. These findings suggest conservation of long-wavelength chlorophylls despite distinct pigment-binding characteristics, shedding light on light-harvesting adaptations in secondary green algae.</p>","PeriodicalId":74192,"journal":{"name":"microPublication biology","volume":"2025 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12364551/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144981624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
microPublication biologyPub Date : 2025-07-28eCollection Date: 2025-01-01DOI: 10.17912/micropub.biology.001633
ByungHoon B Kim
{"title":"Time course measurements of leaf elevation angles during shade avoidance response in <i>Arabidopsis thaliana</i> using <i>Raspberry Pi</i> computers and computer vision technique.","authors":"ByungHoon B Kim","doi":"10.17912/micropub.biology.001633","DOIUrl":"10.17912/micropub.biology.001633","url":null,"abstract":"<p><p>Shade avoidance response in plants includes a higher leaf elevation angle. A cost-effective and noninvasive high throughput image analysis technique was used to measure the dynamics of leaf elevation angles during shade avoidance response in <i>Arabidopsis</i> . Time-lapse images were taken from the top and the side of a plant using <i>Raspberry Pi</i> computers. The leaf elevation index for each plant is determined from the plant dimensions measured by an image analysis software package <i>PlantCV</i> . This method was used to monitor the dynamics of changing leaf elevation angles in wild-type plants and in shade avoidance mutants <i>pif4-2pif5-3</i> and <i>pif7-2</i> plants.</p>","PeriodicalId":74192,"journal":{"name":"microPublication biology","volume":"2025 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12364532/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144981620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
microPublication biologyPub Date : 2025-07-28eCollection Date: 2025-01-01DOI: 10.17912/micropub.biology.001676
Brandon M Waddell, Cheng-Wei Wu
{"title":"Requirement of CSR-1 isoforms and catalytic activity for <i>C. elegans</i> lifespan.","authors":"Brandon M Waddell, Cheng-Wei Wu","doi":"10.17912/micropub.biology.001676","DOIUrl":"10.17912/micropub.biology.001676","url":null,"abstract":"<p><p>The <i>C. elegans</i> CSR-1 encodes an essential Argonaute protein that binds to 22 nucleotide small guide RNA to regulate germline gene expression. Recent characterization of the two CSR-1 isoforms (a and b) have demonstrated tissue-specific expression and functions. Here, we found that loss of function to the <i>csr-1 a</i> isoform has minimal effect on lifespan while a mutant with deletion to both <i>csr-1 a</i> and <i>csr-1 b</i> isoforms shows a significant decrease in lifespan. Furthermore, we found that single copy expression of a slicing inactive variant of <i>csr-1</i> fails to rescue the shortened lifespan. Overall, the data here provide new information on the requirement of isoform and domain-specific contribution of CSR-1 to <i>C. elegans</i> lifespan.</p>","PeriodicalId":74192,"journal":{"name":"microPublication biology","volume":"2025 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12364517/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144981631","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
microPublication biologyPub Date : 2025-07-28eCollection Date: 2025-01-01DOI: 10.17912/micropub.biology.001687
Nirvanjyoti Sharma Shimul, Elena B Benson, Jake P Diaz, Lynn Zavada, Diane C Shakes
{"title":"RMD-3 and RMD-6 identified as new components of the MSP fibrous body complex in <i>C. elegans</i> spermatocytes.","authors":"Nirvanjyoti Sharma Shimul, Elena B Benson, Jake P Diaz, Lynn Zavada, Diane C Shakes","doi":"10.17912/micropub.biology.001687","DOIUrl":"10.17912/micropub.biology.001687","url":null,"abstract":"<p><p>The RMD (regulator of microtubule dynamics) protein family is conserved across various species but their activity and role in spermatogenesis is largely unexplored. Here we report developing an antibody against the two nearly identical proteins <i>C. elegans</i> RMD-3 and RMD-6 . This antibody detects RMD-3 /6 in both immunocytology and western blots. RMD-3 /6 colocalizes with the major sperm protein MSP to the fibrous bodies of spermatocytes, cytoplasm of spermatids, and pseudopods of spermatozoa. RMD-3 /6 are sperm-specific, yet male fertility in triple <i>rmd-2 / rmd-3 / rmd-6</i> knockout mutants is unaffected under conditions tested.</p>","PeriodicalId":74192,"journal":{"name":"microPublication biology","volume":"2025 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12364515/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144981599","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"A polymorphic inframe deletion in the ODR-10 extracellular loop 2 abolishes diacetyl sensing.","authors":"Aatira Mehraj, Rémy Mimbré, Katie Pelletier, Varsha Singh, Marie-Anne Félix","doi":"10.17912/micropub.biology.001722","DOIUrl":"10.17912/micropub.biology.001722","url":null,"abstract":"<p><p>The <i>C. elegans</i> wild strain DL226 carries a 30 bp inframe deletion in the <i>odr-10</i> gene coding for the diacetyl olfactory receptor. DL226 animals are defective for attraction to diacetyl but not to pyrrole, an unrelated odorant also sensed by AWA neurons. Using genome editing in the N2 background, we show that this inframe deletion is causal for the defect in diacetyl sensing. The deletion specifically removes the predicted ligand-binding extracellular loop 2 (ECL2).</p>","PeriodicalId":74192,"journal":{"name":"microPublication biology","volume":"2025 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12368358/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144981448","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}