What the papers say. Genes controlling specific cell fates inC. elegans embryos

BioEssays ◽  
1992 ◽  
Vol 14 (10) ◽  
pp. 705-708 ◽  
Author(s):  
Lois G. Edgar
Keyword(s):  
Specific Cell ◽  
Cell Fates

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 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 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 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.

scholarly journals Cycling in a crowd: coordination of plant cell division, growth, and cell fate

2021 ◽  
Author(s):  
Robert Sablowski ◽  
Crisanto Gutierrez
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Cell Fate ◽  
Plant Cell ◽  
Cell Cycle Progression ◽  
Specific Cell ◽  
Cell Fates ◽  
Cycle Progression ◽  
Cell Divisions ◽  
Major Player

Abstract The reiterative organogenesis that drives plant growth relies on the constant production of new cells, which remain encased by interconnected cell walls. For these reasons, plant morphogenesis strictly depends on the rate and orientation of both cell division and cell growth. Important progress has been made in recent years in understanding how cell cycle progression and the orientation of cell divisions are coordinated with cell and organ growth and with the acquisition of specialized cell fates. We review basic concepts and players in plant cell cycle and division, and then focus on their links to growth-related cues, such as metabolic state, cell size, cell geometry, and cell mechanics, and on how cell cycle progression and cell division are linked to specific cell fates. The retinoblastoma pathway has emerged as a major player in the coordination of the cell cycle with both growth and cell identity, while microtubule dynamics are central in the coordination of oriented cell divisions. Future challenges include clarifying feedbacks between growth and cell cycle progression, revealing the molecular basis of cell division orientation in response to mechanical and chemical signals, and probing the links between cell fate changes and chromatin dynamics during the cell cycle.

The zebrafish colourless gene regulates development of non-ectomesenchymal neural crest derivatives

Development ◽  
2000 ◽  
Vol 127 (3) ◽  
pp. 515-525 ◽  
Author(s):  
R.N. Kelsh ◽  
J.S. Eisen
Keyword(s):  
Nervous System ◽  
Neural Crest ◽  
Cell Types ◽  
Pigment Cells ◽  
Specific Cell ◽  
Zebrafish Embryos ◽  
Craniofacial Skeleton ◽  
Cell Fates ◽  
Peripheral Neurons ◽  
Neural Crest Development

Neural crest forms four major categories of derivatives: pigment cells, peripheral neurons, peripheral glia, and ectomesenchymal cells. Some early neural crest cells generate progeny of several fates. How specific cell fates become specified is still poorly understood. Here we show that zebrafish embryos with mutations in the colourless gene have severe defects in most crest-derived cell types, including pigment cells, neurons and specific glia. In contrast, craniofacial skeleton and medial fin mesenchyme are normal. These observations suggest that colourless has a key role in development of non-ectomesenchymal neural crest fates, but not in development of ectomesenchymal fates. Thus, the cls mutant phenotype reveals a segregation of ectomesenchymal and non-ectomesenchymal fates during zebrafish neural crest development. The combination of pigmentation and enteric nervous system defects makes colourless mutations a model for two human neurocristopathies, Waardenburg-Shah syndrome and Hirschsprung's disease.

Mouse patched1 controls body size determination and limb patterning

Development ◽  
1999 ◽  
Vol 126 (20) ◽  
pp. 4431-4440 ◽  
Author(s):  
L. Milenkovic ◽  
L.V. Goodrich ◽  
K.M. Higgins ◽  
M.P. Scott
Keyword(s):  
Sonic Hedgehog ◽  
Protein A ◽  
Limb Bud ◽  
Specific Cell ◽  
Cell Fates ◽  
Limb Patterning ◽  
Normal Morphology ◽  
Early Embryonic Lethality ◽  
Metallothionein Promoter ◽  
Animal Size

Hedgehog (Hh) proteins control many developmental events by inducing specific cell fates or regulating cell proliferation. The Patched1 (Ptc1) protein, a binding protein for Hh molecules, appears to oppose Hh signals by repressing transcription of genes that can be activated by Hh. Sonic hedgehog (Shh), one of the vertebrate homologs of Hh, controls patterning and growth of the limb but the early embryonic lethality of ptc1(−)(/)(−) mice obscures the roles of ptc1 in later stages of development. We partially rescued ptc1 homozygous mutant embryos using a metallothionein promoter driving ptc1. In a wild-type background, the transgene causes a marked decrease in animal size starting during embryogenesis, and loss of anterior digits. In ptc1 homozygotes, a potent transgenic insert allowed survival to E14 and largely normal morphology except for midbrain overgrowth. A less potent transgene gave rise to partially rescued embryos with massive exencephaly, and polydactyly and branched digits in the limbs. The polydactyly was preceded by unexpected anterior limb bud transcription of Shh, so one function of ptc1 is to repress Shh expression in the anterior limb bud.

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