scholarly journals Mesenchymal condensation-dependent accumulation of collagen VI stabilizes organ-specific cell fates during embryonic tooth formation

2015 ◽  
Vol 244 (6) ◽  
pp. 713-723 ◽  
Author(s):  
Tadanori Mammoto ◽  
Akiko Mammoto ◽  
Amanda Jiang ◽  
Elisabeth Jiang ◽  
Basma Hashmi ◽  
...  
Keyword(s):  
Specific Cell ◽  
Collagen Vi ◽  
Cell Fates ◽  
Tooth Formation ◽  
Organ Specific ◽  
Mesenchymal Condensation

scholarly journals Histone Acetyltransferases and Stem Cell Identity

Cancers ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 2407
Author(s):  
Ruicen He ◽  
Arthur Dantas ◽  
Karl Riabowol
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Cell Fate ◽  
Epigenetic Modification ◽  
Cell Types ◽  
Histone Acetyltransferases ◽  
Specific Cell ◽  
Cell Fates ◽  
Cell Identity ◽  
Hematopoietic Stem

Acetylation of histones is a key epigenetic modification involved in transcriptional regulation. The addition of acetyl groups to histone tails generally reduces histone-DNA interactions in the nucleosome leading to increased accessibility for transcription factors and core transcriptional machinery to bind their target sequences. There are approximately 30 histone acetyltransferases and their corresponding complexes, each of which affect the expression of a subset of genes. Because cell identity is determined by gene expression profile, it is unsurprising that the HATs responsible for inducing expression of these genes play a crucial role in determining cell fate. Here, we explore the role of HATs in the maintenance and differentiation of various stem cell types. Several HAT complexes have been characterized to play an important role in activating genes that allow stem cells to self-renew. Knockdown or loss of their activity leads to reduced expression and or differentiation while particular HATs drive differentiation towards specific cell fates. In this study we review functions of the HAT complexes active in pluripotent stem cells, hematopoietic stem cells, muscle satellite cells, mesenchymal stem cells, neural stem cells, and cancer stem cells.

Drosophila betaHeavy-spectrin is essential for development and contributes to specific cell fates in the eye

Development ◽  
1998 ◽  
Vol 125 (11) ◽  
pp. 2125-2134 ◽  
Author(s):  
G.H. Thomas ◽  
D.C. Zarnescu ◽  
A.E. Juedes ◽  
M.A. Bales ◽  
A. Londergan ◽  
...  
Keyword(s):  
Membrane Skeleton ◽  
Specific Cell ◽  
Cell Integrity ◽  
Cell Fates ◽  
Gene Encoding ◽  
Rhodamine Phalloidin ◽  
Morphological Defects ◽  
Egg Chambers ◽  
Alpha Spectrin ◽  
Cell Cell

The spectrin membrane skeleton is a ubiquitous cytoskeletal structure with several cellular roles, including the maintenance of cell integrity, determination of cell shape and as a contributor to cell polarity. We have isolated mutations in the gene encoding βHeavy-spectrin in Drosophila, and have named this essential locus karst. karst mutant individuals have a pleiotropic phenotype characterized by extensive larval lethality and, in adult escapers, rough eyes, bent wings, tracheal defects and infertility. Within karst mutant eyes, a significant number of ommatidia specifically lack photoreceptor R7 alongside more complex morphological defects. Immunolocalization of betaHeavy-spectrin in wild-type eye-antennal and wing imaginal discs reveals that betaHeavy-spectrin is present in a restricted subdomain of the membrane skeleton that colocalizes with DE-cadherin. We propose a model where normal levels of Sevenless signaling are dependent on tight cell-cell adhesion facilitated by the betaHeavy-spectrin membrane skeleton. Immunolocalization of betaHeavy-spectrin in the adult and larval midgut indicates that it is a terminal web protein, but we see no gross morphological defects in the adult apical brush border in karst mutant flies. Rhodamine phalloidin staining of karst mutant ovaries similarly reveals no conspicuous defect in the actin cytoskeleton or cellular morphology in egg chambers. This is in contrast to mutations in alpha-spectrin, the molecular partner of betaHeavy-spectrin, which affect cellular structure in both the larval gut and adult ovaries. Our results emphasize the fundamental contribution of the spectrin membrane skeleton to normal development and reveals a critical interplay between the integrity of a cell's membrane skeleton, the structure of cell-cell contacts and cell signaling.

scholarly journals Analyzing Impetus of Regenerative Cellular Therapeutics in Myocardial Infarction

2020 ◽  
Vol 9 (5) ◽  
pp. 1277 ◽  
Author(s):  
Ming-Long Chang ◽  
Yu-Jui Chiu ◽  
Jian-Sing Li ◽  
Khoot-Peng Cheah ◽  
Hsiu-Hu Lin
Keyword(s):  
Myocardial Infarction ◽  
Stem Cells ◽  
Cardiac Fibroblasts ◽  
Cell Lineage ◽  
Specific Cell ◽  
Paracrine Factors ◽  
Differentiation Potential ◽  
Cell Based Therapy ◽  
Organ Specific ◽  
Made In

Both vasculature and myocardium in the heart are excessively damaged following myocardial infarction (MI), hence therapeutic strategies for treating MI hearts should concurrently aim for true cardiac repair by introducing new cardiomyocytes to replace lost or injured ones. Of them, mesenchymal stem cells (MSCs) have long been considered a promising candidate for cell-based therapy due to their unspecialized, proliferative differentiation potential to specific cell lineage and, most importantly, their capacity of secreting beneficial paracrine factors which further promote neovascularization, angiogenesis, and cell survival. As a consequence, the differentiated MSCs could multiply and replace the damaged tissues to and turn into tissue- or organ-specific cells with specialized functions. These cells are also known to release potent anti-fibrotic factors including matrix metalloproteinases, which inhibit the proliferation of cardiac fibroblasts, thereby attenuating fibrosis. To achieve the highest possible therapeutic efficacy of stem cells, the other interventions, including hydrogels, electrical stimulations, or platelet-derived biomaterials, have been supplemented, which have resulted in a narrow to broad range of outcomes. Therefore, this article comprehensively analyzed the progress made in stem cells and combinatorial therapies to rescue infarcted myocardium.

scholarly journals The C. elegans heterochronic gene lin-28 coordinates the timing of hypodermal and somatic gonadal programs for hermaphrodite reproductive system morphogenesis

2018 ◽  
Author(s):  
Sungwook Choi ◽  
Victor Ambros
Keyword(s):  
Control Cell ◽  
Gonad Development ◽  
Developmental Timing ◽  
Specific Cell ◽  
Cell Fates ◽  
C Elegans ◽  
Gonad Morphology ◽  
Somatic Gonad ◽  
Heterochronic Gene ◽  
A Cell

AbstractC. elegans heterochronic genes determine the timing of expression of specific cell fates in particular stages of developing larva. However, their broader roles in coordinating developmental events across diverse tissues has been less well investigated. Here, we show that loss of lin-28, a central heterochronic regulator of hypodermal development, causes reduced fertility associated with abnormal somatic gonad morphology. In particular, the abnormal spermatheca-uterine valve morphology of lin-28(lf) hermaphrodites trap embryos in the spermatheca, which disrupts ovulation and causes embryonic lethality. The same genes that act downstream of lin-28 in the regulation of hypodermal developmental timing also act downstream of lin-28 in somatic gonad morphogenesis and fertility. Importantly, we find that hypodermal expression, but not somatic gonadal expression, of lin-28 is sufficient for restoring normal somatic gonad morphology in lin-28(lf) mutants. We propose that the abnormal somatic gonad morphogenesis of lin-28(lf) hermaphrodites results from temporal discoordination between the accelerated hypodermal development and normally timed somatic gonad development. Thus, our findings exemplify how a cell-intrinsic developmental timing program can also control cell non-autonomous signaling critical for proper development of other interacting tissues.

Modifications of cell fate specification in equal-cleaving nemertean embryos: alternate patterns of spiralian development

Development ◽  
1995 ◽  
Vol 121 (10) ◽  
pp. 3175-3185 ◽  
Author(s):  
M.Q. Martindale ◽  
J.Q. Henry
Keyword(s):  
Cell Fate ◽  
Cell Lineage ◽  
Cell Types ◽  
Embryonic Cell ◽  
Specific Cell ◽  
Cell Fate Specification ◽  
Cell Fates ◽  
Developmental Potential ◽  
Fate Specification ◽  
Symmetry Properties

The nemerteans belong to a phylum of coelomate worms that display a highly conserved pattern of cell divisions referred to as spiral cleavage. It has recently been shown that the fates of the four embryonic cell quadrants in two species of nemerteans are not homologous to those in other spiralian embryos, such as the annelids and molluscs (Henry, J. Q. and Martindale, M. Q. (1994a) Develop. Genetics 15, 64–78). Equal-cleaving molluscs utilize inductive interactions to establish quadrant-specific cell fates and embryonic symmetry properties following fifth cleavage. In order to elucidate the manner in which cell fates are established in nemertean embryos, we have conducted cell isolation and deletion experiments to examine the developmental potential of the early cleavage blastomeres of two equal-cleaving nemerteans, Nemertopsis bivittata and Cerebratulus lacteus. These two species display different modes of development: N. bivittata develops directly via a non-feeding larvae, while C. lacteus develops to form a feeding pilidium larva which undergoes a radical metamorphosis to give rise to the juvenile worm. By examining the development of certain structures and cell types characteristic of quadrant-specific fates for each of these species, we have shown that isolated blastomeres of the indirect-developing nemertean, C. lacteus, are capable of generating cell fates that are not a consequence of that cell's normal developmental program. For instance, dorsal blastomeres can form muscle fibers when cultured in isolation. In contrast, isolated blastomeres of the direct-developing species, N. bivittata do not regulate their development to the same extent. Some cell fates are specified in a precocious manner in this species, such as those that give rise to the eyes. Thus, these findings indicate that equal-cleaving spiralian embryos can utilize different mechanisms of cell fate and axis specification. The implications of these patterns of nemertean development are discussed in relation to experimental work in other spiralian embryos, and a model is presented that accounts for possible evolutionary changes in cell lineage and the process of cell fate specification amongst these protostome phyla.

scholarly journals Self-reactive B Cells Are Not Eliminated or Inactivated by Autoantigen Expressed on Thyroid Epithelial Cells

1997 ◽  
Vol 186 (12) ◽  
pp. 2005-2012 ◽  
Author(s):  
Srinivas Akkaraju ◽  
Karen Canaan ◽  
Christopher C. Goodnow
Keyword(s):  
B Cells ◽  
Epithelial Cells ◽  
Thyroid Stimulating Hormone ◽  
Specific Cell ◽  
Cell Repertoire ◽  
Thyroid Cells ◽  
Organ Specific ◽  
Membrane Antigens ◽  
Specific Antigens ◽  
Humoral Tolerance

Graves' Disease results from the production of autoantibodies against receptors for thyroid stimulating hormone (TSH) on thyroid epithelial cells, and represents the prototype for numerous autoimmune diseases caused by autoantibodies that bind to organ-specific cell membrane antigens. To study how humoral tolerance is normally maintained to organ-specific membrane antigens, transgenic mice were generated selectively expressing membrane-bound hen egg lysozyme (mHEL) on the thyroid epithelium. In contrast to the deletion of autoreactive B cells triggered by systemic mHEL (Hartley, S.B., J. Crosbie, R. Brink, A.B. Kantor, A. Basten, and C.C. Goodnow. 1991. Nature. 353:765–769), selective expression of mHEL autoantigen on thyroid cells did not trigger elimination or inactivation of circulating HEL-reactive B cells. These results provide evidence that tolerance is not actively acquired to organ-specific antigens in the preimmune B cell repertoire, underscoring the importance of maintaining tolerance to such antigens by other mechanisms. The role of an intact endothelial barrier in sequestering organ-specific antigens from circulating preimmune B cells is discussed.

scholarly journals Mosaic Analysis of the Liguleless3 Mutant Phenotype in Maize by Coordinate Suppression of Mutator-insertion Alleles

Genetics ◽  
1996 ◽  
Vol 143 (1) ◽  
pp. 489-503 ◽  
Author(s):  
John E Fowler ◽  
Gary J Muehlbauer ◽  
Michael Freeling
Keyword(s):  
Regional Identity ◽  
Transverse Dimension ◽  
Mutant Phenotype ◽  
Specific Cell ◽  
Wild Type ◽  
Cell Fates ◽  
Active Line ◽  
Genetic Mosaic ◽  
Mosaic Analysis ◽  
Cell Autonomy

Abstract Ligubless3-O (Lg3-O) transforms the leaf blade, auricle and ligule into sheath around the midrib region. We conducted a genetic mosaic analysis of the Lg3 phenotype to determine the site of Lg3 gene action. Combining the Mutator (Mu) suppressible Lg3-Or211 and al-mum2 alleles in a Mu-active background generated a stock wherein somatic loss of Mu activity resulted in anthocyanin-marked clonal sectors expressing Lg3 in the leaf. Lg3-Or211 plants appear wild type in a Mu-active line, but Mu-inactive plants express a severe Lg3 phenotype. We observed four sector classes: wild type, sheath-like with ligule displacement, sheath-like with ectopic ligule, and auricle-like. The mutation does not cause transformation to a specific cell or regional identity. Lg3-Or211 activity in the mesophyll alters wild-type epidermal cell fates; activity in epidermis seems funtionless. Lg3 mutant activity has a nonautonomous, cell-layer-specific function in the transverse dimension. In the lateral dimension, sectors of Lg3 mutant phenotype can exhibit either cell-autonomous or nonautonomous effects. Our work demonstrates that mosaic analysis by coordinate suppression of Mu-induced alleles is useful for analyzing the cell autonomy of genetically defined functions.

scholarly journals Arkadia via SNON enables NODAL-SMAD2/3 signaling effectors to transcribe different genes depending on their levels

2018 ◽  
Author(s):  
Jonathon M. Carthy ◽  
Marilia Ioannou ◽  
Vasso Episkopou
Keyword(s):  
Cell Fate ◽  
Target Genes ◽  
Embryonic Stem ◽  
Null Mouse ◽  
Specific Cell ◽  
Cell Fates ◽  
Mammalian Embryo ◽  
Cell Fate Decisions ◽  
Dependent Cell ◽  
Anterior Posterior

AbstractHow cells assess levels of signaling and select to transcribe different target genes depending on the levels of activated effectors remains elusive. High NODAL-signalling levels specify anterior/head, lower specify posterior, and complete loss abolishes anterior-posterior patterning in the mammalian embryo. Here we show that cells assess NODAL-activated SMAD2 and SMAD3 (SMAD2/3) effector-levels by complex formation and pairing each effector with the co-repressor SNON, which is present in the cell before signaling. These complexes enable the E3-ubiquitin ligase Arkadia (RNF111) to degrade SNON. High SMAD2/3 levels can saturate and remove SNON, leading to derepression and activation of a subset of targets (high targets) that are highly susceptible to SNON repression. However, low SMAD2/3 levels can only reduce SNON preventing derepression/activation of high targets. Arkadia degrades SNON transiently only upon signaling exposure, leading to dynamic signaling-responses, which most likely initiate level-specific cell-fate decisions. Arkadia-null mouse embryos and Embryonic Stem Cells (ESC) cannot develop anterior tissues and head. However, SnoN/Arkadia, double-null embryos and ESCs are rescued confirming that Arkadia removes SNON, to achieve level-dependent cell-fatesOne Sentence SummarySignaling intensity induces equivalent degradation of a transcriptional repressor leading to level-dependent responses.

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