Pub Date : 2021-04-22DOI: 10.1101/2021.04.22.440894
Hyung Chul Lee, Cato Hastings, Nidia M.M. Oliveira, R. Pérez-Carrasco, Karen M. Page, Lewis Wolpert, Claudio D. Stern
In many developing and regenerating systems, tissue pattern is established through gradients of informative morphogens, but we know little about how cells interpret these. Using experimental manipulation of early chick embryos including misexpression of an inducer (VG1 or ACTIVIN) and an inhibitor (BMP4), we test two alternative models for their ability to explain how the site of primitive streak formation is positioned relative to the rest of the embryo. In one model, cells read morphogen concentrations cell-autonomously. In the other, cells sense changes in morphogen status relative to their neighbourhood. We find that only the latter model can account for the experimental results, including some counter-intuitive predictions. This mechanism (which we name “neighbourhood watch” model) illuminates the classic “French Flag Problem” and how positional information is interpreted by a sheet of cells in a large developing system. Summary statement In a large developing system, the chick embryo before gastrulation, cells interpret gradients of positional signals relative to their neighbours to position the primitive streak, establishing bilateral symmetry.
{"title":"‘Neighbourhood watch’ model: embryonic epiblast cells assess positional information in relation to their neighbours","authors":"Hyung Chul Lee, Cato Hastings, Nidia M.M. Oliveira, R. Pérez-Carrasco, Karen M. Page, Lewis Wolpert, Claudio D. Stern","doi":"10.1101/2021.04.22.440894","DOIUrl":"https://doi.org/10.1101/2021.04.22.440894","url":null,"abstract":"In many developing and regenerating systems, tissue pattern is established through gradients of informative morphogens, but we know little about how cells interpret these. Using experimental manipulation of early chick embryos including misexpression of an inducer (VG1 or ACTIVIN) and an inhibitor (BMP4), we test two alternative models for their ability to explain how the site of primitive streak formation is positioned relative to the rest of the embryo. In one model, cells read morphogen concentrations cell-autonomously. In the other, cells sense changes in morphogen status relative to their neighbourhood. We find that only the latter model can account for the experimental results, including some counter-intuitive predictions. This mechanism (which we name “neighbourhood watch” model) illuminates the classic “French Flag Problem” and how positional information is interpreted by a sheet of cells in a large developing system. Summary statement In a large developing system, the chick embryo before gastrulation, cells interpret gradients of positional signals relative to their neighbours to position the primitive streak, establishing bilateral symmetry.","PeriodicalId":77105,"journal":{"name":"Development (Cambridge, England). Supplement","volume":"14 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85331410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-04-09DOI: 10.1101/2021.04.08.438913
O. Tidswell, Matthew A. Benton, M. Akam
In Drosophila, segmentation genes of the gap class form a regulatory network that positions segment boundaries and assigns segment identities. This gene network shows striking parallels with another gene network known as the neuroblast timer series. The neuroblast timer genes hunchback, Krüppel, nubbin, and castor are expressed in temporal sequence in neural stem cells to regulate the fate of their progeny. These same four genes are expressed in corresponding spatial sequence along the Drosophila blastoderm. The first two, hunchback and Krüppel, are canonical gap genes, but nubbin and castor have limited or no roles in Drosophila segmentation. Whether nubbin and castor regulate segmentation in insects with the ancestral, sequential mode of segmentation remains largely unexplored. We have investigated the expression and functions of nubbin and castor during segment patterning in the sequentially-segmenting beetle Tribolium. Using multiplex fluorescent in situ hybridisation, we show that Tc-hunchback, Tc-Krüppel, Tc-nubbin and Tc-castor are expressed sequentially in the segment addition zone of Tribolium, in the same order as they are expressed in Drosophila neuroblasts. Furthermore, simultaneous disruption of multiple genes reveals that Tc-nubbin regulates segment identity, but does so redundantly with two previously described gap/gap-like genes, Tc-giant and Tc-knirps. Knockdown of two or more of these genes results in the formation of up to seven pairs of ectopic legs on abdominal segments. We show that this homeotic transformation is caused by loss of abdominal Hox gene expression, likely due to expanded Tc-Krüppel expression. Our findings support the theory that the neuroblast timer series was co-opted for use in insect segment patterning, and contribute to our growing understanding of the evolution and function of the gap gene network outside of Drosophila.
{"title":"The neuroblast timer gene nubbin exhibits functional redundancy with gap genes to regulate segment identity in Tribolium","authors":"O. Tidswell, Matthew A. Benton, M. Akam","doi":"10.1101/2021.04.08.438913","DOIUrl":"https://doi.org/10.1101/2021.04.08.438913","url":null,"abstract":"In Drosophila, segmentation genes of the gap class form a regulatory network that positions segment boundaries and assigns segment identities. This gene network shows striking parallels with another gene network known as the neuroblast timer series. The neuroblast timer genes hunchback, Krüppel, nubbin, and castor are expressed in temporal sequence in neural stem cells to regulate the fate of their progeny. These same four genes are expressed in corresponding spatial sequence along the Drosophila blastoderm. The first two, hunchback and Krüppel, are canonical gap genes, but nubbin and castor have limited or no roles in Drosophila segmentation. Whether nubbin and castor regulate segmentation in insects with the ancestral, sequential mode of segmentation remains largely unexplored. We have investigated the expression and functions of nubbin and castor during segment patterning in the sequentially-segmenting beetle Tribolium. Using multiplex fluorescent in situ hybridisation, we show that Tc-hunchback, Tc-Krüppel, Tc-nubbin and Tc-castor are expressed sequentially in the segment addition zone of Tribolium, in the same order as they are expressed in Drosophila neuroblasts. Furthermore, simultaneous disruption of multiple genes reveals that Tc-nubbin regulates segment identity, but does so redundantly with two previously described gap/gap-like genes, Tc-giant and Tc-knirps. Knockdown of two or more of these genes results in the formation of up to seven pairs of ectopic legs on abdominal segments. We show that this homeotic transformation is caused by loss of abdominal Hox gene expression, likely due to expanded Tc-Krüppel expression. Our findings support the theory that the neuroblast timer series was co-opted for use in insect segment patterning, and contribute to our growing understanding of the evolution and function of the gap gene network outside of Drosophila.","PeriodicalId":77105,"journal":{"name":"Development (Cambridge, England). Supplement","volume":"241 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75777307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-04-02DOI: 10.1101/2021.03.31.437948
Megan Franke, Adam L. Maclean
Cells do not function in isolation. Arguably, every cell fate decision occurs in response to environmental signals. In many cases cell-cell communication alters the dynamics of a cell’s internal gene regulatory network to initiate cell fate transitions, yet models rarely take this into account. Here we develop a multiscale perspective to study the granulocyte-monocyte vs. megakaryocyte-erythrocyte fate decisions. This transition is dictated by the GATA1-PU.1 network, a classical example of a bistable cell fate system. We show that, for a wide range of cell communication topologies, even subtle changes in signaling can have pronounced effects on cell fate decisions. We go on to show how cell-cell coupling through signaling can spontaneously break the symmetry of a homogenous cell population. Noise, both intrinsic and extrinsic, shapes the decision landscape profoundly, and affects the transcriptional dynamics underlying this important hematopoietic cell fate decision-making system.
{"title":"A single-cell resolved cell-cell communication model explains lineage commitment in hematopoiesis","authors":"Megan Franke, Adam L. Maclean","doi":"10.1101/2021.03.31.437948","DOIUrl":"https://doi.org/10.1101/2021.03.31.437948","url":null,"abstract":"Cells do not function in isolation. Arguably, every cell fate decision occurs in response to environmental signals. In many cases cell-cell communication alters the dynamics of a cell’s internal gene regulatory network to initiate cell fate transitions, yet models rarely take this into account. Here we develop a multiscale perspective to study the granulocyte-monocyte vs. megakaryocyte-erythrocyte fate decisions. This transition is dictated by the GATA1-PU.1 network, a classical example of a bistable cell fate system. We show that, for a wide range of cell communication topologies, even subtle changes in signaling can have pronounced effects on cell fate decisions. We go on to show how cell-cell coupling through signaling can spontaneously break the symmetry of a homogenous cell population. Noise, both intrinsic and extrinsic, shapes the decision landscape profoundly, and affects the transcriptional dynamics underlying this important hematopoietic cell fate decision-making system.","PeriodicalId":77105,"journal":{"name":"Development (Cambridge, England). Supplement","volume":"447 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77041361","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-03-28DOI: 10.1101/2021.03.26.437151
Ping Kao, Michael A. Schon, M. Mosiolek, Michael D. Nodine
Soon after fertilization of egg and sperm, plant genomes become transcriptionally activated and drive a series of coordinated cell divisions to form the basic body plan during embryogenesis. Early embryonic cells rapidly diversify from each other, and investigation of the corresponding gene expression dynamics can help elucidate underlying cellular differentiation programs. However, current plant embryonic transcriptome datasets either lack cell-specific information or have RNA contamination from surrounding non-embryonic tissues. We have coupled fluorescence-activated nuclei sorting together with single-nucleus mRNA sequencing to construct a gene expression atlas of Arabidopsis thaliana early embryos at single-cell resolution. In addition to characterizing cell-specific transcriptomes, we found evidence that distinct epigenetic and transcriptional regulatory mechanisms operate across emerging embryonic cell types. These datasets and analyses, as well as the approach we devised, are expected to facilitate the discovery of molecular mechanisms underlying pattern formation in plant embryos. Summary statement A transcriptome atlas of Arabidopsis embryos constructed from single nuclei reveals cell-specific epigenetic and transcriptional regulatory features.
{"title":"Gene expression variation in Arabidopsis embryos at single-nucleus resolution","authors":"Ping Kao, Michael A. Schon, M. Mosiolek, Michael D. Nodine","doi":"10.1101/2021.03.26.437151","DOIUrl":"https://doi.org/10.1101/2021.03.26.437151","url":null,"abstract":"Soon after fertilization of egg and sperm, plant genomes become transcriptionally activated and drive a series of coordinated cell divisions to form the basic body plan during embryogenesis. Early embryonic cells rapidly diversify from each other, and investigation of the corresponding gene expression dynamics can help elucidate underlying cellular differentiation programs. However, current plant embryonic transcriptome datasets either lack cell-specific information or have RNA contamination from surrounding non-embryonic tissues. We have coupled fluorescence-activated nuclei sorting together with single-nucleus mRNA sequencing to construct a gene expression atlas of Arabidopsis thaliana early embryos at single-cell resolution. In addition to characterizing cell-specific transcriptomes, we found evidence that distinct epigenetic and transcriptional regulatory mechanisms operate across emerging embryonic cell types. These datasets and analyses, as well as the approach we devised, are expected to facilitate the discovery of molecular mechanisms underlying pattern formation in plant embryos. Summary statement A transcriptome atlas of Arabidopsis embryos constructed from single nuclei reveals cell-specific epigenetic and transcriptional regulatory features.","PeriodicalId":77105,"journal":{"name":"Development (Cambridge, England). Supplement","volume":"59 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82911429","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-03-02DOI: 10.1101/2021.03.02.433660
Hirosuke Shiura, R. Ono, Saori Tachibana, T. Kohda, T. Kaneko-Ishino, F. Ishino
The therian-specific gene paternally expressed 10 (Peg10) plays an essential role in placenta formation: Peg10 knockout (KO) mice exhibit early embryonic lethality due to severe placental defects. The PEG10 protein exhibits homology to long terminal repeat (LTR) retrotransposon GAG and POL proteins, therefore mice harboring a mutation in its highly conserved viral aspartic protease motif in the POL-like region were generated because it is essential for LTR retrotransposons/retroviruses. Intriguingly, frequent perinatal lethality, not early embryonic lethality, was observed with fetal and placental growth retardation starting mid-gestation. In the mutant placentas, severe defects were observed in the fetal vasculature, where PEG10 is expressed in the three trophoblast cell layers that surround fetal capillary endothelial cells. Thus, Peg10 has essential roles not only in early placenta formation, but also in placental vasculature maintenance from mid- to late-gestation. This implies that along the feto-maternal placenta interface an interaction occurs between two retrovirus-derived genes, Peg10 and retrotransposon Gag like 1 (Rtl1, also called Peg11), that is essential for the maintenance of fetal capillary endothelial cells. Summary statement Disruption of the highly conserved viral aspartic protease domain in PEG10 causes placental abnormality leading to perinatal lethality in mice.
{"title":"PEG10 viral aspartic protease domain is essential for the maintenance of fetal capillary structure in the mouse placenta","authors":"Hirosuke Shiura, R. Ono, Saori Tachibana, T. Kohda, T. Kaneko-Ishino, F. Ishino","doi":"10.1101/2021.03.02.433660","DOIUrl":"https://doi.org/10.1101/2021.03.02.433660","url":null,"abstract":"The therian-specific gene paternally expressed 10 (Peg10) plays an essential role in placenta formation: Peg10 knockout (KO) mice exhibit early embryonic lethality due to severe placental defects. The PEG10 protein exhibits homology to long terminal repeat (LTR) retrotransposon GAG and POL proteins, therefore mice harboring a mutation in its highly conserved viral aspartic protease motif in the POL-like region were generated because it is essential for LTR retrotransposons/retroviruses. Intriguingly, frequent perinatal lethality, not early embryonic lethality, was observed with fetal and placental growth retardation starting mid-gestation. In the mutant placentas, severe defects were observed in the fetal vasculature, where PEG10 is expressed in the three trophoblast cell layers that surround fetal capillary endothelial cells. Thus, Peg10 has essential roles not only in early placenta formation, but also in placental vasculature maintenance from mid- to late-gestation. This implies that along the feto-maternal placenta interface an interaction occurs between two retrovirus-derived genes, Peg10 and retrotransposon Gag like 1 (Rtl1, also called Peg11), that is essential for the maintenance of fetal capillary endothelial cells. Summary statement Disruption of the highly conserved viral aspartic protease domain in PEG10 causes placental abnormality leading to perinatal lethality in mice.","PeriodicalId":77105,"journal":{"name":"Development (Cambridge, England). Supplement","volume":"23 3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80965858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-03-02DOI: 10.1101/2021.03.02.433562
Zhenni Li, Ayala Sela, Y. Fridman, Lucía Garstka, H. Höfte, S. Savaldi-Goldstein, Sebastian Wolf
The plant steroid hormones brassinosteroids (BRs) regulate growth in part through altering the properties of the cell wall, the extracellular matrix of plant cells. Conversely, cell wall signalling connects the state of cell wall homeostasis to the BR receptor complex and modulates BR activity. Here we report that both pectin-triggered cell wall signalling and impaired BR signalling result in altered cell wall orientation in the Arabidopsis root meristem. BR-induced defects in the orientation of newly placed walls are associated with aberrant localization of the cortical division zone but with normal specification of its positioning. Tissue- specific perturbations of BR signalling revealed that the cellular malfunction is unrelated to previously described whole organ growth defects. Thus, tissue type separates the pleiotropic effects of cell wall/BR signals and highlights their importance during cell wall placement.
{"title":"Optimal BR signalling is required for adequate cell wall orientation in the Arabidopsis root meristem","authors":"Zhenni Li, Ayala Sela, Y. Fridman, Lucía Garstka, H. Höfte, S. Savaldi-Goldstein, Sebastian Wolf","doi":"10.1101/2021.03.02.433562","DOIUrl":"https://doi.org/10.1101/2021.03.02.433562","url":null,"abstract":"The plant steroid hormones brassinosteroids (BRs) regulate growth in part through altering the properties of the cell wall, the extracellular matrix of plant cells. Conversely, cell wall signalling connects the state of cell wall homeostasis to the BR receptor complex and modulates BR activity. Here we report that both pectin-triggered cell wall signalling and impaired BR signalling result in altered cell wall orientation in the Arabidopsis root meristem. BR-induced defects in the orientation of newly placed walls are associated with aberrant localization of the cortical division zone but with normal specification of its positioning. Tissue- specific perturbations of BR signalling revealed that the cellular malfunction is unrelated to previously described whole organ growth defects. Thus, tissue type separates the pleiotropic effects of cell wall/BR signals and highlights their importance during cell wall placement.","PeriodicalId":77105,"journal":{"name":"Development (Cambridge, England). Supplement","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73276985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nora Gigli-Bisceglia, Eva van Zelm, W. Huo, J. Lamers, C. Testerink
Soil salinity is an increasing worldwide problem for agriculture, affecting plant growth and yield. To understand the molecular mechanisms activated in response to salt in plants, we investigated the Catharanthus roseus Receptor like Kinase 1 Like (CrRLK1L) family, which contains well described sensors previously shown to be involved in maintaining and sensing the structural integrity of the cell walls. We found that herk1the1-4 double mutants, lacking the function of the Arabidopsis thaliana Receptor like Kinase HERKULES1 combined with a gain-of-function allele of THESEUS1, phenocopied the phenotypes previously reported in plants lacking FERONIA (FER) function. We report that both fer-4 and herk1the1-4 mutants respond strongly to salt application, resulting in a more intense activation of early and late stress responses. We also show that salt triggers de-methyl esterification of loosely bound pectins, responsible for the activation of several salt response signaling pathways. Addition of calcium chloride or chemically inhibiting pectin methyl esterase (PME) activity reduced activation of the early signaling protein Mitogen Activated Protein Kinase 6 (MPK6) as well as amplitude of salt-induced marker gene induction. MPK6 is required for the full induction of the salt-induced gene expression markers we tested. The sodium specific root halotropism response on the other hand, appears independent of MPK6 or calcium application, and is only mildly influenced by the cell wall sensors FER/HERK1/THE1-4 or alteration of PME activity. We hypothesize a model where salt-triggered modification of pectin requires the functionality of FER alone or the HERK1/THE1 combination to attenuate salt responses. Collectively, our results show the complexity of salt stress responses and salt sensing mechanisms and their connection to cell wall modifications, responsible for several salt response pathways and ultimately plant resilience to salinity.
土壤盐碱化是一个日益严重的全球性农业问题，影响着植物的生长和产量。为了了解植物对盐的反应激活的分子机制，我们研究了Catharanthus roseus Receptor like Kinase 1 like (CrRLK1L)家族，该家族包含之前被证明参与维持和感知细胞壁结构完整性的传感器。我们发现herk1the1-4双突变体缺乏拟南芥受体样激酶HERKULES1的功能，结合了THESEUS1的功能获得等位基因，表型上复制了先前报道的缺乏FERONIA (FER)功能的植物的表型。我们报道，fer4和herk1the1-4突变体对盐的施用反应强烈，导致更强烈的早期和晚期胁迫反应的激活。我们还表明，盐触发松散结合的果胶的去甲基酯化反应，负责激活几种盐反应信号通路。添加氯化钙或化学抑制果胶甲基酯酶(PME)活性降低了早期信号蛋白有丝分裂原活化蛋白激酶6 (MPK6)的激活以及盐诱导标记基因诱导的幅度。MPK6是我们测试的盐诱导基因表达标记的完全诱导所必需的。另一方面，钠特异性根嗜盐性反应似乎与MPK6或钙施用无关，仅受细胞壁传感器FER/HERK1/THE1-4或PME活性改变的轻微影响。我们假设一个模型，其中盐触发的果胶修饰需要FER单独或HERK1/THE1组合的功能来减弱盐反应。总的来说，我们的研究结果表明，盐胁迫反应和盐感知机制的复杂性及其与细胞壁修饰的联系，负责几种盐响应途径和最终植物对盐的恢复力。
{"title":"Arabidopsis root responses to salinity depend on pectin modification and cell wall sensing","authors":"Nora Gigli-Bisceglia, Eva van Zelm, W. Huo, J. Lamers, C. Testerink","doi":"10.1242/dev.200363","DOIUrl":"https://doi.org/10.1242/dev.200363","url":null,"abstract":"Soil salinity is an increasing worldwide problem for agriculture, affecting plant growth and yield. To understand the molecular mechanisms activated in response to salt in plants, we investigated the Catharanthus roseus Receptor like Kinase 1 Like (CrRLK1L) family, which contains well described sensors previously shown to be involved in maintaining and sensing the structural integrity of the cell walls. We found that herk1the1-4 double mutants, lacking the function of the Arabidopsis thaliana Receptor like Kinase HERKULES1 combined with a gain-of-function allele of THESEUS1, phenocopied the phenotypes previously reported in plants lacking FERONIA (FER) function. We report that both fer-4 and herk1the1-4 mutants respond strongly to salt application, resulting in a more intense activation of early and late stress responses. We also show that salt triggers de-methyl esterification of loosely bound pectins, responsible for the activation of several salt response signaling pathways. Addition of calcium chloride or chemically inhibiting pectin methyl esterase (PME) activity reduced activation of the early signaling protein Mitogen Activated Protein Kinase 6 (MPK6) as well as amplitude of salt-induced marker gene induction. MPK6 is required for the full induction of the salt-induced gene expression markers we tested. The sodium specific root halotropism response on the other hand, appears independent of MPK6 or calcium application, and is only mildly influenced by the cell wall sensors FER/HERK1/THE1-4 or alteration of PME activity. We hypothesize a model where salt-triggered modification of pectin requires the functionality of FER alone or the HERK1/THE1 combination to attenuate salt responses. Collectively, our results show the complexity of salt stress responses and salt sensing mechanisms and their connection to cell wall modifications, responsible for several salt response pathways and ultimately plant resilience to salinity.","PeriodicalId":77105,"journal":{"name":"Development (Cambridge, England). Supplement","volume":"37 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75101035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-12-14DOI: 10.1101/2020.12.14.422687
Dhruv Raina, Fiorella Fabris, L. G. Morelli, C. Schröter
Signal transduction networks process extracellular signals to guide cell fate decisions such as to divide, differentiate, or die. These networks can generate characteristic dynamic activities that are shaped by their cell-type specific architecture. The differentiation of pluripotent cells is controlled by FGF/ERK signaling. However, the dynamic activity of the FGF/ERK signaling network in this context remains unexplored. Here we use live cell sensors in wild type and Fgf4 mutant mouse embryonic stem cells to measure ERK dynamic activity in single cells, in response to defined ligand concentrations. We find that ERK activity oscillates in embryonic stem cells. Single cells can transit between oscillatory and non-oscillatory behavior, leading to heterogeneous dynamic activities in the population. Oscillations become more prevalent with increasing FGF4 dose, while maintaining a robust characteristic timescale. Our results suggest that FGF/ERK signaling operates in the vicinity of a transition point between oscillatory and non-oscillatory dynamics in embryonic stem cells.
{"title":"Intermittent ERK oscillations downstream of FGF in mouse embryonic stem cells","authors":"Dhruv Raina, Fiorella Fabris, L. G. Morelli, C. Schröter","doi":"10.1101/2020.12.14.422687","DOIUrl":"https://doi.org/10.1101/2020.12.14.422687","url":null,"abstract":"Signal transduction networks process extracellular signals to guide cell fate decisions such as to divide, differentiate, or die. These networks can generate characteristic dynamic activities that are shaped by their cell-type specific architecture. The differentiation of pluripotent cells is controlled by FGF/ERK signaling. However, the dynamic activity of the FGF/ERK signaling network in this context remains unexplored. Here we use live cell sensors in wild type and Fgf4 mutant mouse embryonic stem cells to measure ERK dynamic activity in single cells, in response to defined ligand concentrations. We find that ERK activity oscillates in embryonic stem cells. Single cells can transit between oscillatory and non-oscillatory behavior, leading to heterogeneous dynamic activities in the population. Oscillations become more prevalent with increasing FGF4 dose, while maintaining a robust characteristic timescale. Our results suggest that FGF/ERK signaling operates in the vicinity of a transition point between oscillatory and non-oscillatory dynamics in embryonic stem cells.","PeriodicalId":77105,"journal":{"name":"Development (Cambridge, England). Supplement","volume":"11 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79091177","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-10-15DOI: 10.1101/2020.10.15.340521
Dongsun Shin, Mitsutoshi Nakamura, Yoshitaka Morishita, Mototsugu Eiraku, Tomoko Yamakawa, Takeshi Sasamura, M. Akiyama, Mikiko Inaki, K. Matsuno
Proper organ development often requires nuclei to move to a specific position within the cell. To determine how nuclear positioning affects left-right (LR) development in the Drosophila anterior midgut (AMG), we developed a surface-modeling method to measure and describe nuclear behavior at stages 13-14, captured in three-dimensional time-lapse movies. We describe the distinctive positioning and a novel collective nuclear behavior by which nuclei align LR-symmetrically along the anterior-posterior axis in the visceral muscles that overlie the midgut and are responsible for this organ’s LR-asymmetric development. Wnt4 signaling is crucial for the collective behavior and proper positioning of the nuclei, as are myosin II and LINC complex, without which the nuclei failed to align LR-symmetrically. The LR-symmetric positioning of the nuclei is important for the subsequent LR-asymmetric development of the AMG. We propose that the bilaterally symmetrical positioning of these nuclei may be mechanically coupled with subsequent LR-asymmetric morphogenesis.
{"title":"Collective nuclear behavior shapes bilateral nuclear symmetry for subsequent left-right asymmetric morphogenesis in Drosophila","authors":"Dongsun Shin, Mitsutoshi Nakamura, Yoshitaka Morishita, Mototsugu Eiraku, Tomoko Yamakawa, Takeshi Sasamura, M. Akiyama, Mikiko Inaki, K. Matsuno","doi":"10.1101/2020.10.15.340521","DOIUrl":"https://doi.org/10.1101/2020.10.15.340521","url":null,"abstract":"Proper organ development often requires nuclei to move to a specific position within the cell. To determine how nuclear positioning affects left-right (LR) development in the Drosophila anterior midgut (AMG), we developed a surface-modeling method to measure and describe nuclear behavior at stages 13-14, captured in three-dimensional time-lapse movies. We describe the distinctive positioning and a novel collective nuclear behavior by which nuclei align LR-symmetrically along the anterior-posterior axis in the visceral muscles that overlie the midgut and are responsible for this organ’s LR-asymmetric development. Wnt4 signaling is crucial for the collective behavior and proper positioning of the nuclei, as are myosin II and LINC complex, without which the nuclei failed to align LR-symmetrically. The LR-symmetric positioning of the nuclei is important for the subsequent LR-asymmetric development of the AMG. We propose that the bilaterally symmetrical positioning of these nuclei may be mechanically coupled with subsequent LR-asymmetric morphogenesis.","PeriodicalId":77105,"journal":{"name":"Development (Cambridge, England). Supplement","volume":"18 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89467229","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-09-15DOI: 10.1101/2020.09.15.296574
A. Rosa, W. Giese, Katja Meier, Silvanus Alt, Alexandra Klaus-Bergmann, Lowell T. Edgar, Eireen Bartels, Russell T Collins, Anna Szymborska, Baptiste Coxam, M. Bernabeu, H. Gerhardt
Endothelial cell migration and proliferation are essential for the establishment of a hierarchical organization of blood vessels and optimal distribution of blood. However, how these cellular processes are coordinated remains unknown. Here, using the zebrafish trunk vasculature we show that in future veins endothelial cells proliferate more than in future arteries and migrate preferentially towards neighboring arteries. In future arteries endothelial cells show a biphasic migration profile. During sprouting cells move away from the dorsal aorta, during remodelling cells stop or move towards the feeding aorta. The final morphology of blood vessels is thus established by local proliferation and oriented cell migration to and from neighboring vessels. Additionally, we identify WASp to be essential for this differential migration. Loss of WASp leads to irregular distribution of endothelial cells, substantially enlarged veins and persistent arteriovenous shunting. Mechanistically, we report that WASp drives the assembly of junctional associated actin filaments and is required for junctional expression of PECAM-1. Together, our data identify that functional vascular patterning in the zebrafish trunk utilizes differential cell movement regulated by junctional actin, and that interruption of differential migration may represent a pathomechanism in vascular malformations.
{"title":"WASp controls oriented migration of endothelial cells to achieve functional vascular patterning","authors":"A. Rosa, W. Giese, Katja Meier, Silvanus Alt, Alexandra Klaus-Bergmann, Lowell T. Edgar, Eireen Bartels, Russell T Collins, Anna Szymborska, Baptiste Coxam, M. Bernabeu, H. Gerhardt","doi":"10.1101/2020.09.15.296574","DOIUrl":"https://doi.org/10.1101/2020.09.15.296574","url":null,"abstract":"Endothelial cell migration and proliferation are essential for the establishment of a hierarchical organization of blood vessels and optimal distribution of blood. However, how these cellular processes are coordinated remains unknown. Here, using the zebrafish trunk vasculature we show that in future veins endothelial cells proliferate more than in future arteries and migrate preferentially towards neighboring arteries. In future arteries endothelial cells show a biphasic migration profile. During sprouting cells move away from the dorsal aorta, during remodelling cells stop or move towards the feeding aorta. The final morphology of blood vessels is thus established by local proliferation and oriented cell migration to and from neighboring vessels. Additionally, we identify WASp to be essential for this differential migration. Loss of WASp leads to irregular distribution of endothelial cells, substantially enlarged veins and persistent arteriovenous shunting. Mechanistically, we report that WASp drives the assembly of junctional associated actin filaments and is required for junctional expression of PECAM-1. Together, our data identify that functional vascular patterning in the zebrafish trunk utilizes differential cell movement regulated by junctional actin, and that interruption of differential migration may represent a pathomechanism in vascular malformations.","PeriodicalId":77105,"journal":{"name":"Development (Cambridge, England). Supplement","volume":"126 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89198593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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