Developmental cellPub Date : 2024-09-09DOI: 10.1016/j.devcel.2024.07.002
Sara Badodi, Silvia Marino
{"title":"Epigenetic reprogramming enables NF1A/B oncogenic role in SHH medulloblastoma","authors":"Sara Badodi, Silvia Marino","doi":"10.1016/j.devcel.2024.07.002","DOIUrl":"https://doi.org/10.1016/j.devcel.2024.07.002","url":null,"abstract":"<p>In this issue of Developmental Cell, Shiraishi et al. investigate the epigenetic changes occurring during the formation of SHH medulloblastoma and show that an epigenomic shift renders Nuclear Factor I family of transcription factors oncogenic.</p>","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":null,"pages":null},"PeriodicalIF":11.8,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142158711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Developmental cellPub Date : 2024-09-09DOI: 10.1016/j.devcel.2024.08.005
Jonathan Dragwidge, Amélie Bernard
{"title":"HOPping to the vacuole: Autophagosome and late endosomes combine to control plant autophagosome degradation","authors":"Jonathan Dragwidge, Amélie Bernard","doi":"10.1016/j.devcel.2024.08.005","DOIUrl":"https://doi.org/10.1016/j.devcel.2024.08.005","url":null,"abstract":"<p>In this issue of <em>Developmental Cell</em>, Jiang et al. report that the Arabidopsis HOPS tethering complex subunit VPS41 acts to catalyze the formation of a degradation pathway composed of a hybrid of autophagosomes and late endosomes.</p>","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":null,"pages":null},"PeriodicalIF":11.8,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142158710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Developmental cellPub Date : 2024-09-03DOI: 10.1016/j.devcel.2024.08.007
Pierre Priam, Veneta Krasteva, Philippe Rousseau, Alexandre Polsinelli, Laurence Côté, Ines Desanlis, Azer Farah, Vincent-Philippe Lavallée, Marie Kmita, Julie A. Lessard
{"title":"Smarcd1 subunit of SWI/SNF chromatin-remodeling complexes collaborates with E2a to promote murine lymphoid specification","authors":"Pierre Priam, Veneta Krasteva, Philippe Rousseau, Alexandre Polsinelli, Laurence Côté, Ines Desanlis, Azer Farah, Vincent-Philippe Lavallée, Marie Kmita, Julie A. Lessard","doi":"10.1016/j.devcel.2024.08.007","DOIUrl":"https://doi.org/10.1016/j.devcel.2024.08.007","url":null,"abstract":"<p>Lymphocyte development from murine hematopoietic stem cells (HSCs) entails a loss of self-renewal capacity and a progressive restriction of developmental potential. Previous research from our laboratory suggests that specialized assemblies of ATP-dependent SWI/SNF chromatin-remodeling complexes play lineage-specific roles during murine hematopoiesis. Here, we demonstrate that the Smarcd1 subunit is essential for specification of lymphoid cell fate from multipotent progenitors. Acute deletion of <em>Smarcd1</em> in murine adult hematopoiesis leads to lymphopenia, characterized by a near-complete absence of early lymphoid progenitors and mature B and T cells, while the myeloid and erythroid lineages remain unaffected. Mechanistically, we demonstrate that Smarcd1 is essential for the coordinated activation of a lymphoid gene signature in murine multipotent progenitors. This is achieved by interacting with the E2a transcription factor at proximal promoters and by regulating the activity of distal enhancers. Globally, these findings identify Smarcd1 as an essential chromatin remodeler that governs lymphoid cell fate.</p>","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":null,"pages":null},"PeriodicalIF":11.8,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142123934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Developmental cellPub Date : 2024-09-03DOI: 10.1016/j.devcel.2024.08.009
Jun-Yeong Ahn, Somi Kim, Chang Rok Kim, Ji-Hyun Lee, Jong Min Kim, Thomas M. Klompstra, Yoon Ha Choi, Yoon Jeon, Yongwoo Na, Jong-Seo Kim, Yuki Okada, Ho Lee, Ik Soo Kim, Jong Kyoung Kim, Bon-Kyoung Koo, Sung Hee Baek
{"title":"Dual function of PHF16 in reinstating homeostasis of murine intestinal epithelium after crypt regeneration","authors":"Jun-Yeong Ahn, Somi Kim, Chang Rok Kim, Ji-Hyun Lee, Jong Min Kim, Thomas M. Klompstra, Yoon Ha Choi, Yoon Jeon, Yongwoo Na, Jong-Seo Kim, Yuki Okada, Ho Lee, Ik Soo Kim, Jong Kyoung Kim, Bon-Kyoung Koo, Sung Hee Baek","doi":"10.1016/j.devcel.2024.08.009","DOIUrl":"https://doi.org/10.1016/j.devcel.2024.08.009","url":null,"abstract":"<p>Intestinal stem cells (ISCs) are highly vulnerable to damage, being in a constant state of proliferation. Reserve stem cells repair the intestinal epithelium following damage-induced ablation of ISCs. Here, we report that the epigenetic regulator plant homology domain (PHD) finger protein 16 (PHF16) restores homeostasis of the intestinal epithelium after initial damage-induced repair. In <em>Phf16</em><sup><em>−/Y</em></sup> mice, revival stem cells (revSCs) showed defects in exiting the regenerative state, and intestinal crypt regeneration failed even though revSCs were still induced in response to tissue damage, as observed by single-cell RNA sequencing (scRNA-seq). Analysis of <em>Phf16</em><sup><em>−/Y</em></sup> intestinal organoids by RNA sequencing (RNA-seq) and ATAC sequencing identified that PHF16 restores homeostasis of the intestinal epithelium by inducing retinoic acid receptor (RAR)/retinoic X receptor (RXR) target genes through HBO1-mediated histone H3K14 acetylation, while at the same time counteracting YAP/TAZ activity by ubiquitination of CDC73. Together, our findings demonstrate the importance of timely suppression of regenerative activity by PHF16 for the restoration of gut homeostasis after acute tissue injury.</p>","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":null,"pages":null},"PeriodicalIF":11.8,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142123933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Developmental cellPub Date : 2024-08-30DOI: 10.1016/j.devcel.2024.08.006
Xubo Niu, Delmy L. Melendez, Suyash Raj, Junming Cai, Dulanjalee Senadeera, Joseph Mandelbaum, Ilya A. Shestopalov, Scott D. Martin, Leonard I. Zon, Thorsten M. Schlaeger, Lick Pui Lai, Andrew P. McMahon, April M. Craft, Jenna L. Galloway
{"title":"A conserved transcription factor regulatory program promotes tendon fate","authors":"Xubo Niu, Delmy L. Melendez, Suyash Raj, Junming Cai, Dulanjalee Senadeera, Joseph Mandelbaum, Ilya A. Shestopalov, Scott D. Martin, Leonard I. Zon, Thorsten M. Schlaeger, Lick Pui Lai, Andrew P. McMahon, April M. Craft, Jenna L. Galloway","doi":"10.1016/j.devcel.2024.08.006","DOIUrl":"https://doi.org/10.1016/j.devcel.2024.08.006","url":null,"abstract":"<p>Tendons, which transmit force from muscles to bones, are highly prone to injury. Understanding the mechanisms driving tendon fate would impact efforts to improve tendon healing, yet this knowledge is limited. To find direct regulators of tendon progenitor emergence, we performed a zebrafish high-throughput chemical screen. We established forskolin as a tenogenic inducer across vertebrates, functioning through Creb1a, which is required and sufficient for tendon fate. Putative enhancers containing cyclic AMP (cAMP) response elements (CREs) in humans, mice, and fish drove specific expression in zebrafish cranial and fin tendons. Analysis of these genomic regions identified motifs for early B cell factor (Ebf/EBF) transcription factors. Mutation of CRE or Ebf/EBF motifs significantly disrupted enhancer activity and specificity in tendons. Zebrafish <em>ebf1a/ebf3a</em> mutants displayed defects in tendon formation. Notably, Creb1a/CREB1 and Ebf1a/Ebf3a/EBF1 overexpression facilitated tenogenic induction in zebrafish and human pluripotent stem cells. Together, our work identifies the functional conservation of two transcription factors in promoting tendon fate.</p>","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":null,"pages":null},"PeriodicalIF":11.8,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142100895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Developmental cellPub Date : 2024-08-28DOI: 10.1016/j.devcel.2024.08.004
Liu Yang, Audrey Zhu, Javed M. Aman, David Denberg, Marcus D. Kilwein, Robert A. Marmion, Alex N.T. Johnson, Alexey Veraksa, Mona Singh, Martin Wühr, Stanislav Y. Shvartsman
{"title":"ERK synchronizes embryonic cleavages in Drosophila","authors":"Liu Yang, Audrey Zhu, Javed M. Aman, David Denberg, Marcus D. Kilwein, Robert A. Marmion, Alex N.T. Johnson, Alexey Veraksa, Mona Singh, Martin Wühr, Stanislav Y. Shvartsman","doi":"10.1016/j.devcel.2024.08.004","DOIUrl":"https://doi.org/10.1016/j.devcel.2024.08.004","url":null,"abstract":"<p>Extracellular-signal-regulated kinase (ERK) signaling controls development and homeostasis and is genetically deregulated in human diseases, including neurocognitive disorders and cancers. Although the list of ERK functions is vast and steadily growing, the full spectrum of processes controlled by any specific ERK activation event remains unknown. Here, we show how ERK functions can be systematically identified using targeted perturbations and global readouts of ERK activation. Our experimental model is the <em>Drosophila</em> embryo, where ERK signaling at the embryonic poles has thus far only been associated with the transcriptional patterning of the future larva. Through a combination of live imaging and phosphoproteomics, we demonstrated that ERK activation at the poles is also critical for maintaining the speed and synchrony of embryonic cleavages. The presented approach to interrogating phosphorylation networks identifies a hidden function of a well-studied signaling event and sets the stage for similar studies in other organisms.</p>","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":null,"pages":null},"PeriodicalIF":11.8,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142085752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Secreted PTEN binds PLXDC2 on macrophages to drive antitumor immunity and tumor suppression","authors":"Cheng Zhang, Hong-Ming Ma, Shuai Wu, Jia-Ming Shen, Na Zhang, Yi-Lu Xu, Cheng-Xiao Li, Ping He, Meng-Kai Ge, Xi-Li Chu, Yu-Xue Zhang, Jun-Ke Zheng, Guo-Qiang Chen, Shao-Ming Shen","doi":"10.1016/j.devcel.2024.08.003","DOIUrl":"https://doi.org/10.1016/j.devcel.2024.08.003","url":null,"abstract":"<p>Loss of phosphatase and tensin homolog (PTEN) has been linked to an immunosuppressive tumor microenvironment, but its underlying mechanisms remain largely enigmatic. Here, we report that PTEN can be secreted by the transmembrane emp24 domain-containing protein 10 (TMED10)-channeled protein secretion pathway. Inhibiting PTEN secretion from tumor cells contributes to immunosuppression and impairs the tumor-suppressive role of PTEN, while intratumoral injection of PTEN protein promotes antitumor immunity and suppresses tumor growth in mice. Mechanistically, extracellular PTEN binds to the plexin domain-containing protein 2 (PLXDC2) on macrophages, triggering subsequent activation of JAK2-STAT1 signaling, which switches tumor-associated macrophages (TAMs) from the immunosuppressive to inflammatory phenotype, leading to enhanced activation of CD8<sup>+</sup> T and natural killer cells. Importantly, PTEN treatment also enhances the therapeutic efficacy of anti-PD-1 treatment in mice and reverses the immune-suppressive phenotype of patient-derived primary TAMs. These data identify a cytokine-like role of PTEN in immune activation and tumor suppression and demonstrate the therapeutic potential for extracellular administration of PTEN in cancer immunotherapy.</p>","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":null,"pages":null},"PeriodicalIF":11.8,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142084968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Developmental cellPub Date : 2024-08-23DOI: 10.1016/j.devcel.2024.08.001
Mariana Romeiro Motta, François Nédélec, Helen Saville, Elke Woelken, Claire Jacquerie, Martine Pastuglia, Sara Christina Stolze, Eveline Van De Slijke, Lev Böttger, Katia Belcram, Hirofumi Nakagami, Geert De Jaeger, David Bouchez, Arp Schnittger
{"title":"The cell cycle controls spindle architecture in Arabidopsis by activating the augmin pathway.","authors":"Mariana Romeiro Motta, François Nédélec, Helen Saville, Elke Woelken, Claire Jacquerie, Martine Pastuglia, Sara Christina Stolze, Eveline Van De Slijke, Lev Böttger, Katia Belcram, Hirofumi Nakagami, Geert De Jaeger, David Bouchez, Arp Schnittger","doi":"10.1016/j.devcel.2024.08.001","DOIUrl":"https://doi.org/10.1016/j.devcel.2024.08.001","url":null,"abstract":"<p><p>To ensure an even segregation of chromosomes during somatic cell division, eukaryotes rely on mitotic spindles. Here, we measured prime characteristics of the Arabidopsis mitotic spindle and built a three-dimensional dynamic model using Cytosim. We identified the cell-cycle regulator CYCLIN-DEPENDENT KINASE B1 (CDKB1) together with its cyclin partner CYCB3;1 as key regulators of spindle morphology in Arabidopsis. We found that the augmin component ENDOSPERM DEFECTIVE1 (EDE1) is a substrate of the CDKB1;1-CYCB3;1 complex. A non-phosphorylatable mutant rescue of ede1 resembled the spindle phenotypes of cycb3;1 and cdkb1 mutants and the protein associated less efficiently with spindle microtubules. Accordingly, reducing the level of augmin in simulations recapitulated the phenotypes observed in the mutants. Our findings emphasize the importance of cell-cycle-dependent phospho-control of the mitotic spindle in plant cells and support the validity of our model as a framework for the exploration of mechanisms controlling the organization of the eukaryotic spindle.</p>","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":null,"pages":null},"PeriodicalIF":10.7,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142079652","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"tRNA-m<sup>1</sup>A methylation controls the infection of Magnaporthe oryzae by supporting ergosterol biosynthesis.","authors":"Rongrong He, Ziwei Lv, Yinan Li, Shuchao Ren, Jiaqi Cao, Jun Zhu, Xinrong Zhang, Huimin Wu, Lihao Wan, Ji Tang, Shutong Xu, Xiao-Lin Chen, Zhipeng Zhou","doi":"10.1016/j.devcel.2024.08.002","DOIUrl":"https://doi.org/10.1016/j.devcel.2024.08.002","url":null,"abstract":"<p><p>Ergosterols are essential components of fungal plasma membranes. Inhibitors targeting ergosterol biosynthesis (ERG) genes are critical for controlling fungal pathogens, including Magnaporthe oryzae, the fungus that causes rice blast. However, the translational mechanisms governing ERG gene expression remain largely unexplored. Here, we show that the Trm6/Trm61 complex catalyzes dynamic N<sup>1</sup>-methyladenosine at position 58 (m<sup>1</sup>A58) in 51 transfer RNAs (tRNAs) of M. oryzae, significantly influencing translation at both the initiation and elongation stages. Notably, tRNA m<sup>1</sup>A58 promotes elongation speed at most cognate codons mainly by enhancing eEF1-tRNA binding rather than affecting tRNA abundance or charging. The absence of m<sup>1</sup>A58 leads to substantial decreases in the translation of ERG genes, ergosterol production, and, consequently, fungal virulence. Simultaneously targeting the Trm6/Trm61 complex and the ergosterol biosynthesis pathway markedly improves rice blast control. Our findings demonstrate an important role of m<sup>1</sup>A58-mediated translational regulation in ergosterol production and fungal infection, offering a potential strategy for fungicide development.</p>","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":null,"pages":null},"PeriodicalIF":10.7,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142079653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Developmental cellPub Date : 2024-08-22DOI: 10.1016/j.devcel.2024.07.021
Alina L. Li, Kensuke Sugiura, Noriyuki Nishiwaki, Kensuke Suzuki, Dorsay Sadeghian, Jun Zhao, Anirban Maitra, David Falvo, Rohit Chandwani, Jason R. Pitarresi, Peter A. Sims, Anil K. Rustgi
{"title":"FRA1 controls acinar cell plasticity during murine KrasG12D-induced pancreatic acinar to ductal metaplasia","authors":"Alina L. Li, Kensuke Sugiura, Noriyuki Nishiwaki, Kensuke Suzuki, Dorsay Sadeghian, Jun Zhao, Anirban Maitra, David Falvo, Rohit Chandwani, Jason R. Pitarresi, Peter A. Sims, Anil K. Rustgi","doi":"10.1016/j.devcel.2024.07.021","DOIUrl":"https://doi.org/10.1016/j.devcel.2024.07.021","url":null,"abstract":"<p>Acinar cells have been proposed as a cell-of-origin for pancreatic ductal adenocarcinoma (PDAC) after undergoing acinar-to-ductal metaplasia (ADM). ADM can be triggered by pancreatitis, causing acinar cells to de-differentiate to a ductal-like state. We identify FRA1 (gene name <em>Fosl1</em>) as the most active transcription factor during <em>Kras</em><sup><em>G12D</em></sup> acute pancreatitis-mediated injury, and we have elucidated a functional role of FRA1 by generating an acinar-specific <em>Fosl1</em> knockout mouse expressing <em>Kras</em><sup><em>G12D</em></sup>. Using a gene regulatory network and pseudotime trajectory inferred from single-nuclei ATAC-seq and bulk RNA sequencing (RNA-seq), we hypothesized a regulatory model of the acinar-ADM-pancreatic intraepithelial neoplasia (PanIN) continuum and experimentally validated that <em>Fosl1</em> knockout mice are delayed in the onset of ADM and neoplastic transformation. Our study also identifies that pro-inflammatory cytokines, such as granulocyte colony stimulating factor (G-CSF), can regulate FRA1 activity to modulate ADM. Our findings identify that FRA1 is a mediator of acinar cell plasticity and is critical for acinar cell de-differentiation and transformation.</p>","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":null,"pages":null},"PeriodicalIF":11.8,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142023033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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