Biology OpenPub Date : 2025-02-15Epub Date: 2025-02-24DOI: 10.1242/bio.061825
Cameron T Dixon, Pamela Yang, Kimberly McCall
{"title":"Traumatic injury leads to ovarian cell death and reproductive disturbances in Drosophila melanogaster.","authors":"Cameron T Dixon, Pamela Yang, Kimberly McCall","doi":"10.1242/bio.061825","DOIUrl":"10.1242/bio.061825","url":null,"abstract":"<p><p>Traumatic injury (TI), or global blunt force trauma, can arise from many sources such as car crashes, sports and intimate partner violence. Effects from these injuries impact the whole organism and can lead to many different pathologies, such as inflammation, neurodegeneration, gut dysbiosis, and female reproductive detriments. Drosophila melanogaster has recently emerged as a powerful model to study traumatic injuries due to their high conservation of physiological effects post-trauma and the genetic toolset that they leverage. Previously, we reported female-specific reproductive deficits post mild TI in Drosophila. Here we investigate the effects of more severe trauma on females and found an increased retention of mature eggs and decrease in egg laying. Additionally, severe trauma led to an increase of midstage egg chamber death and formation of melanization, a known marker of immune activation. These studies provide a valuable invertebrate model to understand disturbances to female reproduction post-trauma.</p>","PeriodicalId":9216,"journal":{"name":"Biology Open","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11892359/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143432407","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Biology OpenPub Date : 2025-02-15Epub Date: 2025-02-12DOI: 10.1242/bio.061840
María Nazareth González Alvarado, Jessica Aprato
{"title":"Sox8: a multifaceted transcription factor in development and disease.","authors":"María Nazareth González Alvarado, Jessica Aprato","doi":"10.1242/bio.061840","DOIUrl":"10.1242/bio.061840","url":null,"abstract":"<p><p>Sox8 is a transcription factor that belongs to the Sox family of high-mobility-group domain containing proteins and is closely related to Sox9 and Sox10. During prenatal development, Sox8 is expressed in several ectoderm-, endoderm- and mesoderm-derived tissues and has been implicated in processes of organogenesis and differentiation. Sox8 expression is found in several important cells such as Sertoli cells in the male gonad, glial cells, satellite cells, and chondrocytes. However, Sox8 is not essential for the proper development of any of the involved systems, as it functions redundantly with Sox9 or Sox10 and no major developmental disturbances have been noticed in its absence. Despite its perceived limited importance as a developmental regulator, Sox8 exhibits a more significant role in late development and adult tissues. Several studies highlight the importance of Sox8 for the homeostasis of adipose tissue, Sertoli cells and the blood-testis-barrier functioning, and the maintenance of myelin in the central nervous system. Emerging evidence points to SOX8 as a promising candidate for a disease-causing gene in humans and suggests that changes in SOX8 function or expression could contribute to pathological states. For instance, genetic variants of SOX8 have been linked to multiple sclerosis and familial essential tremor, while SOX8 alterations have been related to poor cancer prognosis and infertility. This Review provides an overview of Sox8's versatile role in development and adult tissues as well as its lesser-known contributions to various diseases, and its potential as a therapeutic target.</p>","PeriodicalId":9216,"journal":{"name":"Biology Open","volume":"14 2","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11849977/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143398127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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 story of Biology Open: a conversation with past and present Editors-in-Chief.","authors":"Saanjbati Adhikari, Alejandra Clark, Rachel Hackett","doi":"10.1242/bio.061897","DOIUrl":"10.1242/bio.061897","url":null,"abstract":"","PeriodicalId":9216,"journal":{"name":"Biology Open","volume":"14 2","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11892354/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143499298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Biology OpenPub Date : 2025-02-15Epub Date: 2025-02-06DOI: 10.1242/bio.061828
Ariadna Carol Illa, Henning Hvid, Torben Elm, Christa Andsbjerg Frederiksen, Lonnie Frimodt Bangshof, Dennis Funch Danielsen, Søren Skov, Carsten Dan Ley
{"title":"From early development to maturity: a phenotypic analysis of the Townes sickle cell disease mice.","authors":"Ariadna Carol Illa, Henning Hvid, Torben Elm, Christa Andsbjerg Frederiksen, Lonnie Frimodt Bangshof, Dennis Funch Danielsen, Søren Skov, Carsten Dan Ley","doi":"10.1242/bio.061828","DOIUrl":"10.1242/bio.061828","url":null,"abstract":"<p><p>Well-characterised mouse models of disease may provide valuable insights into pathophysiology. This study characterises the Townes mouse model of sickle cell disease (SCD) and establishes a time window in which the disease is present but does not progress significantly in terms of severity. We examined Townes mice with the HbAA, HbAS, and HbSS genotypes from young (4 weeks) to mature (5 months) stages of life to assess the disease state at different ages and any progression. We conducted blood tests, histological organ damage evaluations, and metabolic assessments to identify a suitable time frame for study based on welfare considerations. Townes HbSS mice displayed key SCD features such as anaemia, haemolysis, thromboinflammation and organ pathology. Notably, these manifestations remained relatively stable over the study period, indicating a stable phase suitable for conducting intervention studies. Mice with HbAS and HbAA genotypes served as comparative controls, showing minimal to no pathology throughout. These findings are valuable for future research on SCD and may ultimately lead to the development of more effective treatments for this debilitating disease.</p>","PeriodicalId":9216,"journal":{"name":"Biology Open","volume":"14 2","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11832121/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143254703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Biology OpenPub Date : 2025-02-15Epub Date: 2025-01-30DOI: 10.1242/bio.061811
Wangsun Choi, Dennis Goldfarb, Feng Yan, Michael B Major, Alan S Fanning, Mark Peifer
{"title":"Proximity proteomics provides a new resource for exploring the function of Afadin and the complexity of cell-cell adherens junctions.","authors":"Wangsun Choi, Dennis Goldfarb, Feng Yan, Michael B Major, Alan S Fanning, Mark Peifer","doi":"10.1242/bio.061811","DOIUrl":"10.1242/bio.061811","url":null,"abstract":"<p><p>The network of proteins at the interface between cell-cell adherens junctions and the actomyosin cytoskeleton provides robust yet dynamic connections that facilitate cell shape change and motility. While this was initially thought to be a simple linear connection via classic cadherins and their associated catenins, we now have come to appreciate that many more proteins are involved, providing robustness and mechanosensitivity. Defining the full set of proteins in this network remains a key objective in our field. Proximity proteomics provides a means to define these networks. Mammalian Afadin and its Drosophila homolog Canoe are key parts of this protein network, facilitating diverse cell shape changes during gastrulation and other events of embryonic morphogenesis. Here we report results of several proximity proteomics screens, defining proteins in the neighborhood of both the N- and C-termini of mammalian Afadin in the premier epithelial model, MDCK cells. We compare our results with previous screens done in other cell types, and with proximity proteomics efforts with other junctional proteins. These reveal the value of multiple screens in defining the full network of neighbors and offer interesting insights into the overlap in protein composition between different epithelial cell junctions.</p>","PeriodicalId":9216,"journal":{"name":"Biology Open","volume":"14 2","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11810119/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Biology OpenPub Date : 2025-02-15Epub Date: 2025-02-04DOI: 10.1242/bio.061647
Carmen Daems, El-Sayed Baz, Rudi D'Hooge, Zsuzsanna Callaerts-Végh, Patrick Callaerts
{"title":"Gene expression differences in the olfactory bulb associated with differential social interactions and olfactory deficits in Pax6 heterozygous mice.","authors":"Carmen Daems, El-Sayed Baz, Rudi D'Hooge, Zsuzsanna Callaerts-Végh, Patrick Callaerts","doi":"10.1242/bio.061647","DOIUrl":"10.1242/bio.061647","url":null,"abstract":"<p><p>Mutations in the highly conserved Pax6 transcription factor have been implicated in neurodevelopmental disorders and behavioral abnormalities, yet the mechanistic basis of the latter remain poorly understood. Our study, using behavioral phenotyping, has identified aberrant social interactions, characterized by withdrawal behavior, and olfactory deficits in Pax6 heterozygous mutant mice. The molecular mechanisms underlying the observed phenotypes were characterized by means of RNA-sequencing on isolated olfactory bulbs followed by validation with qRT-PCR. Comparative analysis of olfactory bulb transcriptomes further reveals an imbalance between neuronal excitation and inhibition, synaptic dysfunction, and alterations in epigenetic regulation as possible mechanisms underlying the abnormal social behavior. We observe a considerable overlap with autism-associated genes and suggest that studying Pax6-dependent gene regulatory networks may further our insight into molecular mechanisms implicated in autistic-like behaviors in Pax6 mutations, thereby paving the way for future research in this area.</p>","PeriodicalId":9216,"journal":{"name":"Biology Open","volume":"14 2","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11832127/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143122358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Biology OpenPub Date : 2025-02-15Epub Date: 2025-01-30DOI: 10.1242/bio.061601
Brennan M Mercola, Tatiana V Villalobos, Jocelyn E Wood, Ankita Basu, Alyssa E Johnson
{"title":"Increased expression of the small lysosomal gene SVIP in the Drosophila gut suppresses pathophysiological features associated with a high-fat diet.","authors":"Brennan M Mercola, Tatiana V Villalobos, Jocelyn E Wood, Ankita Basu, Alyssa E Johnson","doi":"10.1242/bio.061601","DOIUrl":"10.1242/bio.061601","url":null,"abstract":"<p><p>Lysosomes are digestive organelles that are crucial for nutrient sensing and metabolism. Lysosome impairment is linked to a broad spectrum of metabolic disorders, underscoring their importance to human health. Thus, lysosomes are an attractive target for metabolic disease therapies. In previous work, we discovered a novel class of tubular lysosomes that are morphologically and functionally distinct from traditionally described vesicular lysosomes. Tubular lysosomes are present in multiple tissues, are broadly conserved from invertebrates to mammals, are more proficient at degrading autophagic cargo than vesicular lysosomes, and delay signs of tissue aging when induced ectopically. Thus, triggering tubular lysosome formation presents one mechanism to increase lysosome activity and, notably, overproduction of the small lysosomal protein, SVIP, is a robust genetic strategy for triggering lysosomal tubulation on demand. In this study, we examine whether SVIP overexpression in the fly gut can suppress pathophysiological phenotypes associated with an obesogenic high-fat diet. Indeed, our results indicate that increasing SVIP expression in the fly gut reduces lipid accumulation, suppresses body mass increase, and improves survival in flies fed a high-fat diet. Collectively, these data hint that increasing lysosomal activity through induction of tubular lysosomal networks, could be one strategy to combat obesity-related pathologies.</p>","PeriodicalId":9216,"journal":{"name":"Biology Open","volume":"14 2","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11810118/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Biology OpenPub Date : 2025-02-15Epub Date: 2025-02-06DOI: 10.1242/bio.061644
Sweta Jha, Johanna Pispa, Carina I Holmberg
{"title":"Impairment of proteasome-associated deubiquitinating enzyme Uchl5/UBH-4 affects autophagy.","authors":"Sweta Jha, Johanna Pispa, Carina I Holmberg","doi":"10.1242/bio.061644","DOIUrl":"10.1242/bio.061644","url":null,"abstract":"<p><p>The autophagy-lysosomal pathway (ALP) and the ubiquitin-proteasome system (UPS) are the two major intracellular proteolytic systems that mediate protein turnover in eukaryotes. Although a crosstalk exists between these two systems, it is still unclear how UPS and ALP interact in vivo. Here, we investigated how impaired function of the proteasome-associated deubiquitinating enzyme (DUB) Uchl5/UBH-4 affects autophagy in human cells and in a multicellular organism. We show that downregulation of Uchl5 by siRNA reduces autophagy by partially blocking the fusion of autophagosomes with the lysosomes in HeLa cells, which is similar to a previously reported role of the proteasome-associated DUB Usp14 on autophagy. However, exposure of Caenorhabditis elegans to ubh-4 or usp-14 RNAi, or to their pharmacological inhibitors, results in diverse effects on numbers of autophagosomes and autolysosomes, without blocking the lysosomal fusion, in the intestine, hypodermal seam cells and the pharynx. Our results reveal that impairment of Uchl5/UBH-4 and Usp14 affects autophagy in a tissue context manner. A deeper insight into the interplay between UPS and ALP in various tissues in vivo has the potential to promote development of therapeutic approaches for disorders associated with proteostasis dysfunction.</p>","PeriodicalId":9216,"journal":{"name":"Biology Open","volume":"14 2","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11832120/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143254714","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Biology OpenPub Date : 2025-02-15Epub Date: 2025-02-20DOI: 10.1242/bio.061674
Victoria Hyland, M Kathryn Iovine
{"title":"Ccn2a acts downstream of cx43 to influence joint formation during zebrafish fin regeneration.","authors":"Victoria Hyland, M Kathryn Iovine","doi":"10.1242/bio.061674","DOIUrl":"10.1242/bio.061674","url":null,"abstract":"<p><p>This study provides new insights into the molecular pathways dictating skeletal patterning during zebrafish fin regeneration. Connexin43 (Cx43) is known to influence skeletal patterning by inhibiting evx1 expression and thereby regulating the timing of joint formation. Here, we demonstrate that cellular communication network factor 2 (ccn2a) also contributes to this pathway. We find that Ccn2a appears to act downstream of Cx43 and similarly inhibits joint formation by inhibiting evx1 expression. Pharmacological inhibition of β-catenin demonstrates that ccn2a is likely regulated by β-catenin. Additionally, this paper provides evidence that Yap signaling contributes to joint formation through regulating ccn2a. These findings provide novel insights into the role of Ccn2a during skeletal patterning.</p>","PeriodicalId":9216,"journal":{"name":"Biology Open","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11876838/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143439919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}