scholarly journals Mago Nashi Is Essential for Spermatogenesis in Marsilea

2007 ◽  
Vol 18 (10) ◽  
pp. 3711-3722 ◽  
Author(s):  
Corine M. van der Weele ◽  
Chia-Wei Tsai ◽  
Stephen M. Wolniak
Keyword(s):  
Cell Fate ◽  
De Novo ◽  
Exon Junction Complex ◽  
Protein Distribution ◽  
Stored Mrna ◽  
Asymmetric Divisions ◽  
Core Components ◽  
Conserved Gene ◽  
Tubulin Protein ◽  
Mago Nashi

Spermatogenesis in Marsilea vestita is a rapid process that is activated by placing dry microspores into water. Nine division cycles produce seven somatic cells and 32 spermatids, where size and position define identity. Spermatids undergo de novo formation of basal bodies in a particle known as a blepharoplast. We are interested in mechanisms responsible for spermatogenous initial formation. Mago nashi (Mv-mago) is a highly conserved gene present as stored mRNA and stored protein in the microspore. Mv-mago protein increases in abundance during development and it localizes at discrete cytoplasmic foci (Mago-dots). RNA interference experiments show that new Mv-mago protein is required for development. With Mv-mago silenced, asymmetric divisions become symmetric, cell fate is disrupted, and development stops. The α-tubulin protein distribution, centrin translation, and Mv-PRP19 mRNA distribution are no longer restricted to the spermatogenous cells. Centrin aggregations, resembling blepharoplasts, occur in jacket cells. Mago-dots are undetectable after the silencing of Mv-mago, Mv-Y14, or Mv-eIF4AIII, three core components of the exon junction complex (EJC), suggesting that Mago-dots are either EJCs in the cytoplasm, or Mv-mago protein aggregations dependent on EJCs. Mv-mago protein and other EJC components apparently function in cell fate determination in developing male gametophytes of M. vestita.

A regulatory network of microRNAs confers lineage commitment during early developmental trajectories of B and T lymphocytes

2021 ◽  
Vol 118 (46) ◽  
pp. e2104297118
Author(s):  
Sameena Nikhat ◽  
Anurupa D. Yadavalli ◽  
Arpita Prusty ◽  
Priyanka K. Narayan ◽  
Dasaradhi Palakodeti ◽  
...  
Keyword(s):  
Gene Expression ◽  
T Lymphocytes ◽  
Cell Fate ◽  
T Lymphocyte ◽  
De Novo ◽  
Gene Expression Pattern ◽  
Lymphocyte Development ◽  
Motif Analysis ◽  
Differentiation Potential ◽  
B And T Lymphocytes

The commitment of hematopoietic multipotent progenitors (MPPs) toward a particular lineage involves activation of cell type–specific genes and silencing of genes that promote alternate cell fates. Although the gene expression programs of early–B and early–T lymphocyte development are mutually exclusive, we show that these cell types exhibit significantly correlated microRNA (miRNA) profiles. However, their corresponding miRNA targetomes are distinct and predominated by transcripts associated with natural killer, dendritic cell, and myeloid lineages, suggesting that miRNAs function in a cell-autonomous manner. The combinatorial expression of miRNAs miR-186-5p, miR-128-3p, and miR-330-5p in MPPs significantly attenuates their myeloid differentiation potential due to repression of myeloid-associated transcripts. Depletion of these miRNAs caused a pronounced de-repression of myeloid lineage targets in differentiating early–B and early–T cells, resulting in a mixed-lineage gene expression pattern. De novo motif analysis combined with an assay of promoter activities indicates that B as well as T lineage determinants drive the expression of these miRNAs in lymphoid lineages. Collectively, we present a paradigm that miRNAs are conserved between developing B and T lymphocytes, yet they target distinct sets of promiscuously expressed lineage-inappropriate genes to suppress the alternate cell-fate options. Thus, our studies provide a comprehensive compendium of miRNAs with functional implications for B and T lymphocyte development.

scholarly journals p38-MAPK mediated rRNA processing and translation regulation enables PrE differentiation during mouse blastocyst maturation

2020 ◽  
Author(s):  
Pablo Bora ◽  
Lenka Gahurova ◽  
Tomáš Mašek ◽  
Andrea Hauserova ◽  
David Potěšil ◽  
...  
Keyword(s):  
Cell Fate ◽  
P38 Mapk ◽  
Ribosomal Proteins ◽  
De Novo ◽  
Inner Cell Mass ◽  
Cell Mass ◽  
Translation Regulation ◽  
Placental Development ◽  
Mapk Activity ◽  
Live Embryo

AbstractBackgroundp38-MAPKs are stress-activated kinases necessary for placental development and nutrient and oxygen transfer during murine post-implantation development. In preimplantation development, p38-MAPK activity is required for blastocyst formation. Additionally, we have previously reported its role in regulating specification of inner cell mass (ICM) towards primitive endoderm (PrE), although a comprehensive mechanistic understanding is currently limited. Adopting live embryo imaging, proteomic and transcriptomic approaches, we report experimental data that directly address this deficit.ResultsChemical inhibition of p38-MAPK activity during blastocyst maturation causes impaired blastocyst cavity expansion, most evident between the third and tenth hours post inhibition onset. We identify an overlapping minimal early blastocyst maturation window of p38-MAPKi inhibition (p38-MAPKi) sensitivity, that is sufficient to impair PrE cell fate by the late blastocyst (E4.5) stage. Comparative proteomic analyses reveal substantial downregulation of ribosomal proteins, the mRNA transcripts of which are also significantly upregulated. Ontological analysis of the differentially expressed transcriptome during this developmental period reveals “translation” related gene transcripts as being most significantly, yet transiently, affected by p38-MAPKi. Moreover, combined assays consistently report concomitant reductions in de novo translation that are associated with accumulation of unprocessed rRNA precursors. Using a phosphoproteomic approach, ± p38-MAPKi, we identified Mybpp1a, an rRNA transcription and processing regulator gene, as a potential p38-MAPK effector. We report that siRNA mediated clonal knockdown of Mybpp1a is associated with significantly diminished PrE contribution. Lastly, we show that defective PrE specification caused by p38-MAPKi (but not MEK/ERK signalling inhibition) can be partially rescued by activating the archetypal mTOR mediated translation regulatory pathway.ConclusionsActivated p38-MAPK controls blastocyst maturation in an early and distinctly transient developmental window by regulating gene functionalities related to translation, that creates a permissive environment for appropriate specification of ICM cell fate.

De novo induction of the organizer and formation of the primitive streak in an experimental model of notochord reconstitution in avian embryos

Development ◽  
1998 ◽  
Vol 125 (2) ◽  
pp. 201-213 ◽  
Author(s):  
S. Yuan ◽  
G.C. Schoenwolf
Keyword(s):  
Cell Fate ◽  
De Novo ◽  
Primitive Streak ◽  
Model System ◽  
Floor Plate ◽  
Avian Embryos ◽  
New Information ◽  
Derivatives Of ◽  
Novel Model ◽  
Neurula Stage

We have developed a model system for analyzing reconstitution of the notochord using cultured blastoderm isolates lacking Hensen's node and the primitive streak. Despite lacking normal notochordal precursor cells, the notochord still forms in these isolates during the 36 hours in culture. Reconstitution of the notochord involves an inducer, which acts upon a responder, thereby inducing a reconstituted notochord. To better understand the mechanism of notochord reconstitution, we asked whether formation of the notochord in the model system was preceded by reconstitution of Hensen's node, the organizer of the avian neuraxis. Our results show not only that a functional organizer is reconstituted, but that this organizer is induced from the responder. First, fate mapping reveals that the responder forms a density, morphologically similar to Hensen's node, during the first 10–12 hours in culture, and that this density expresses typical markers of Hensen's node. Second, the density, when fate mapped or when labeled and transplanted in place of Hensen's node, forms typical derivatives of Hensen's node such as endoderm, notochord and the floor plate of the neural tube. Third, the density, when transplanted to an ectopic site, induces a secondary neuraxis, identical to that induced by Hensen's node. And fourth, the density acts as a suppressor of notochord reconstitution, as does Hensen's node, when transplanted to other blastoderm isolates. Our results also reveal that the medial edge of the isolate forms a reconstituted primitive streak, which gives rise to the normal derivatives of the definitive primitive streak along its rostrocaudal extent and which expresses typical streak markers. Finally, our results demonstrate that the notochordal inducer also induces the reconstituted Hensen's node and, therefore, acts like a Nieuwkoop Center. These findings increase our understanding of the mechanism of notochord reconstitution, provide new information and a novel model system for studying the induction of the organizer and reveal the potential of the epiblast to regulate its cell fate and patterns of gene expression during late gastrula/early neurula stage in higher vertebrates.

Wingless signaling generates pattern through two distinct mechanisms

Development ◽  
1997 ◽  
Vol 124 (19) ◽  
pp. 3727-3736 ◽  
Author(s):  
R. Hays ◽  
G.B. Gibori ◽  
A. Bejsovec
Keyword(s):  
Cell Fate ◽  
Cellular Response ◽  
Biological Activities ◽  
Essential Feature ◽  
Structural Features ◽  
Protein Distribution ◽  
Wild Type ◽  
Cell Fates ◽  
Amino Acid Region ◽  
Acid Region

wingless (wg) and its vertebrate homologues, the Wnt genes, play critical roles in the generation of embryonic pattern. In the developing Drosophila epidermis, wg is expressed in a single row of cells in each segment, but it influences cell identities in all rows of epidermal cells in the 10- to 12-cell-wide segment. Wg signaling promotes specification of two distinct aspects of the wild-type intrasegmental pattern: the diversity of denticle types present in the anterior denticle belt and the smooth or naked cuticle constituting the posterior surface of the segment. We have manipulated the expression of wild-type and mutant wg transgenes to explore the mechanism by which a single secreted signaling molecule can promote these distinctly different cell fates. We present evidence consistent with the idea that naked cuticle cell fate is specified by a cellular pathway distinct from the denticle diversity-generating pathway. Since these pathways are differentially activated by mutant Wg ligands, we propose that at least two discrete classes of receptor for Wg may exist, each transducing a different cellular response. We also find that broad Wg protein distribution across many cell diameters is required for the generation of denticle diversity, suggesting that intercellular transport of the Wg protein is an essential feature of pattern formation within the epidermal epithelium. Finally, we demonstrate that an 85 amino acid region not conserved in vertebrate Wnts is dispensable for Wg function and we discuss structural features of the Wingless protein required for its distinct biological activities.

scholarly journals Developmental clock and mechanism of de novo polarization of the mouse embryo

Science ◽  
2020 ◽  
Vol 370 (6522) ◽  
pp. eabd2703
Author(s):  
Meng Zhu ◽  
Jake Cornwall-Scoones ◽  
Peizhe Wang ◽  
Charlotte E. Handford ◽  
Jie Na ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cell Fate ◽  
De Novo ◽  
Cell Fate Specification ◽  
Mouse Development ◽  
Fate Specification ◽  
Apical Domain ◽  
Transcription Factor 4 ◽  
Genome Activation ◽  
Zygotic Genome

Embryo polarization is critical for mouse development; however, neither the regulatory clock nor the molecular trigger that it activates is known. Here, we show that the embryo polarization clock reflects the onset of zygotic genome activation, and we identify three factors required to trigger polarization. Advancing the timing of transcription factor AP-2 gamma (Tfap2c) and TEA domain transcription factor 4 (Tead4) expression in the presence of activated Ras homolog family member A (RhoA) induces precocious polarization as well as subsequent cell fate specification and morphogenesis. Tfap2c and Tead4 induce expression of actin regulators that control the recruitment of apical proteins on the membrane, whereas RhoA regulates their lateral mobility, allowing the emergence of the apical domain. Thus, Tfap2c, Tead4, and RhoA are regulators for the onset of polarization and cell fate segregation in the mouse.

Molecular cloning of a centrin homolog from Marsilea vestita and evidence for its translational control during spermiogenesis

1999 ◽  
Vol 77 (2) ◽  
pp. 101-108 ◽  
Author(s):  
Peter E Hart ◽  
Stephen M Wolniak
Keyword(s):  
Translational Control ◽  
De Novo ◽  
Basal Bodies ◽  
Motile Cells ◽  
Marsilea Vestita ◽  
Stored Mrna ◽  
Eukaryotic Organisms ◽  
Alpha Amanitin ◽  
Made In

Spermiogenesis in the water fern Marsilea vestita is a process that reaches completion 11 h after dry microspores are immersed in an aqueous medium at 20°C. Each microspore produces 32 spermatozoids and each spermatozoid has a coiled cell body and approximately 140 cilia. The spermatids make basal bodies de novo, from a structure known as a blepharoplast. From the onset of development, the spores contain a large quantity of protein and stored mRNA. We have found previously that centrin, a protein involved in the function of microtubule organizing centers and present in association with basal bodies in motile cells, is made in large quantity approximately 4 h after the microspores are placed into liquid medium. In this paper, we show that a centrin cDNA (MvCen1) we isolated from M. vestita closely resembles centrin cDNAs from other eukaryotic organisms. MvCen1, synthesized in Escherichia coli as a GST-fusion protein, reacted with anti-centrin monoclonal antibodies on immunoblots. Northern blot analysis demonstrates that centrin mRNA is present in the dry microspore at the time of imbibition, at levels that remain constant over 10 h of development and are unaffected by treatment of spores with alpha-amanitin. The centrin transcripts, stored in dry microspores, cannot be translated in vitro for at least 30 min after imbibition.Key words: Marsilea vestita, spermatozoid, spermiogenesis, centrin, MTOC.

scholarly journals Eph signaling controls mitotic spindle orientation and cell proliferation in neuroepithelial cells

2019 ◽  
Vol 218 (4) ◽  
pp. 1200-1217 ◽  
Author(s):  
Maribel Franco ◽  
Ana Carmena
Keyword(s):  
Cell Proliferation ◽  
Cell Fate ◽  
Mitotic Spindle ◽  
Optic Lobe ◽  
Spindle Orientation ◽  
Intercellular Signaling ◽  
Neuroepithelial Cells ◽  
Core Components ◽  
Conserved Core ◽  
Activity Dependent

Mitotic spindle orientation must be tightly regulated during development and adult tissue homeostasis. It determines cell-fate specification and tissue architecture during asymmetric and symmetric cell division, respectively. Here, we uncover a novel role for Ephrin–Eph intercellular signaling in controlling mitotic spindle alignment in Drosophila optic lobe neuroepithelial cells through aPKC activity–dependent myosin II regulation. We show that conserved core components of the mitotic spindle orientation machinery, including Discs Large1, Mud/NuMA, and Canoe/Afadin, mislocalize in dividing Eph mutant neuroepithelial cells and produce spindle alignment defects in these cells when they are down-regulated. In addition, the loss of Eph leads to a Rho signaling–dependent activation of the PI3K–Akt1 pathway, enhancing cell proliferation within this neuroepithelium. Hence, Eph signaling is a novel extrinsic mechanism that regulates both spindle orientation and cell proliferation in the Drosophila optic lobe neuroepithelium. Similar mechanisms could operate in other Drosophila and vertebrate epithelia.

scholarly journals Resveratrol Targets Sphingolipid Metabolism to Induce Growth Inhibition in FLT3 ITD Acute Myeloid Leukemia

Proceedings ◽  
2019 ◽  
Vol 40 (1) ◽  
pp. 4
Author(s):  
Ersöz ◽  
Adan
Keyword(s):  
Growth Inhibition ◽  
Cell Fate ◽  
De Novo ◽  
Therapeutic Potential ◽  
Annexin V ◽  
Sphingolipid Metabolism ◽  
Ceramide Synthase ◽  
Cytotoxic Effects ◽  
Sphingosine 1 Phosphate ◽  
First Time

Sphingolipids are important signaling lipids which play crucial roles to determine the cell fate. Ceramide, apoptotic central molecule of sphingolipid metabolism, which is produced through de novo pathway by serine palmitoyl transferase (SPT) and can be converted to antiapoptotic sphingosine-1-phosphate (S1P) and glucosyl ceramide (GC) by sphingosine kinase (SK) and glucosyl ceramide synthase (GCS), respectively. It is aimed to investigate therapeutic potential of resveratrol on FLT3-ITD (Internal Tandem Duplication) AML cells and to identify potential mechanism behind resveratrol-mediated growth inhibition by targeting of ceramide metabolism. The cytotoxic effects of resveratrol, SPT inhibitor (myricoin), SK-1 inhibitor (SKI II), GCS inhibitor (PDMP), resveratrol: SPT inhibitor, resveratrol: SK-1 inhibitor and resveratrol: GCS inhibitor combinations on MOLM-13 and MV4-11 FLT3 ITD AML cells were investigated by cell proliferation assay. Apoptosis was evaluated by annexin V/PI double staining. There were synergistic cytotoxic effects of resveratrol with co-administration of SPT inhibitor, SK-1 inhibitor and GCS inhibitor and apoptosis was synergistically induced for resveratrol and its combinations. This preliminary data showed for the first time that resveratrol might inhibit the growth of FLT3 ITD AML cells through targeting ceramide metabolism.

scholarly journals Scd1 controls de novo beige fat biogenesis through succinate-dependent regulation of mitochondrial complex II

2020 ◽  
Vol 117 (5) ◽  
pp. 2462-2472 ◽  
Author(s):  
Keli Liu ◽  
Liangyu Lin ◽  
Qing Li ◽  
Yueqing Xue ◽  
Fanjun Zheng ◽  
...  
Keyword(s):  
Cell Fate ◽  
Metabolic Diseases ◽  
De Novo ◽  
Great Promise ◽  
Mitochondrial Complex ◽  
Differentiation Potential ◽  
Complex Ii ◽  
White Adipocytes ◽  
Beige Adipocytes ◽  
Adipocyte Progenitors

Preadipocytes can give rise to either white adipocytes or beige adipocytes. Owing to their distinct abilities in nutrient storage and energy expenditure, strategies that specifically promote “beiging” of adipocytes hold great promise for counterbalancing obesity and metabolic diseases. Yet, factors dictating the differentiation fate of adipocyte progenitors remain to be elucidated. We found that stearoyl-coenzyme A desaturase 1 (Scd1)-deficient mice, which resist metabolic stress, possess augmentation in beige adipocytes under basal conditions. Deletion of Scd1 in mature adipocytes expressing Fabp4 or Ucp1 did not affect thermogenesis in mice. Rather, Scd1 deficiency shifted the differentiation fate of preadipocytes from white adipogenesis to beige adipogenesis. Such effects are dependent on succinate accumulation in adipocyte progenitors, which fuels mitochondrial complex II activity. Suppression of mitochondrial complex II by Atpenin A5 or oxaloacetic acid reverted the differentiation potential of Scd1-deficient preadipocytes to white adipocytes. Furthermore, supplementation of succinate was found to increase beige adipocyte differentiation both in vitro and in vivo. Our data reveal an unappreciated role of Scd1 in determining the cell fate of adipocyte progenitors through succinate-dependent regulation of mitochondrial complex II.

Composites and Structures for Regenerative Engineering

2014 ◽  
Vol 1621 ◽  
pp. 3-15 ◽  
Author(s):  
Cato T. Laurencin ◽  
Roshan James
Keyword(s):  
Cell Fate ◽  
Soft Tissues ◽  
De Novo ◽  
Control Cell ◽  
Continuous Phase ◽  
Lessons Learned ◽  
Regenerative Capacity ◽  
Regenerative Engineering ◽  
Organ Systems ◽  
Increasing Demand

ABSTRACTRegenerative engineering was conceptualized by bridging the lessons learned in developmental biology and stem cell science with biomaterial constructs and engineering principles to ultimately generate de novo tissue. We seek to incorporate our understanding of natural tissue development to design tissue-inducing biomaterials, structures and composites than can stimulate the regeneration of complex tissues, organs, and organ systems through location-specific topographies and physico-chemical cues incorporated into a continuous phase. This combination of classical top-down tissue engineering approach with bottom-up strategies used in regenerative biology represents a new multidisciplinary paradigm. Advanced surface topographies and material scales are used to control cell fate and the consequent regenerative capacity.Musculoskeletal tissues are critical to the normal functioning of an individual and following damage or degeneration they show extremely limited endogenous regenerative capacity. The increasing demand for biologically compatible donor tissue and organ transplants far outstrips the availability leading to an acute shortage. We have developed several biomimetic structures using various biomaterial platforms to combine optimal mechanical properties, porosity, bioactivity, and functionality to effect repair and regeneration of hard tissues such as bone, and soft tissues such as ligament and tendon. Starting with simple structures, we have developed composite and multi-scale systems that very closely mimic the native tissue architecture and material composition. Ultimately, we aim to modulate the regenerative potential, including proliferation, phenotype maturation, matrix production, and apoptosis through cell-scaffold and host –scaffold interactions developing complex tissues and organ systems.

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