scholarly journals The relationship between cell size and cell fate in Volvox carteri.

1993 ◽  
Vol 123 (1) ◽  
pp. 191-208 ◽  
Author(s):  
M M Kirk ◽  
A Ransick ◽  
S E McRae ◽  
D L Kirk
Keyword(s):  
Cell Size ◽  
Cell Fate ◽  
Somatic Cells ◽  
Large Cell ◽  
Embryonic Cells ◽  
Wild Type ◽  
Volvox Carteri ◽  
Cell Stage ◽  
Cell Specification ◽  
Cytoplasmic Factor

In Volvox carteri development, visibly asymmetric cleavage divisions set apart large embryonic cells that will become asexual reproductive cells (gonidia) from smaller cells that will produce terminally differentiated somatic cells. Three mechanisms have been proposed to explain how asymmetric division leads to cell specification in Volvox: (a) by a direct effect of cell size (or a property derived from it) on cell specification, (b) by segregation of a cytoplasmic factor resembling germ plasm into large cells, and (c) by a combined effect of differences in cytoplasmic quality and cytoplasmic quantity. In this study a variety of V. carteri embryos with genetically and experimentally altered patterns of development were examined in an attempt to distinguish among these hypotheses. No evidence was found for regionally specialized cytoplasm that is essential for gonidial specification. In all cases studied, cells with a diameter > approximately 8 microns at the end of cleavage--no matter where or how these cells had been produced in the embryo--developed as gonidia. Instructive observations in this regard were obtained by three different experimental interventions. (a) When heat shock was used to interrupt cleavage prematurely, so that presumptive somatic cells were left much larger than they normally would be at the end of cleavage, most cells differentiated as gonidia. This result was obtained both with wild-type embryos that had already divided asymmetrically (and should have segregated any cytoplasmic determinants involved in cell specification) and with embryos of a mutant that normally produces only somatic cells. (b) When individual wild-type blastomeres were isolated at the 16-cell stage, both the anterior blastomeres that normally produce two gonidia each and the posterior blastomeres that normally produce no gonidia underwent modified cleavage patterns and each produced an average of one large cell that developed as a gonidium. (c) When large cells were created microsurgically in a region of the embryo that normally makes only somatic cells, these large cells became gonidia. These data argue strongly for a central role of cell size in germ/soma specification in Volvox carteri, but leave open the question of how differences in cell size are actually transduced into differences in gene expression.

scholarly journals Unequal distribution of 16S mtrRNA at the 2-cell stage regulates cell lineage allocations in mouse embryos

Reproduction ◽  
2016 ◽  
Vol 151 (4) ◽  
pp. 351-367 ◽  
Author(s):  
Zhuxia Zheng ◽  
Hongmei Li ◽  
Qinfen Zhang ◽  
Lele Yang ◽  
Huayu Qi
Keyword(s):  
Cell Fate ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Cell Lineage ◽  
Early Embryogenesis ◽  
Embryonic Cells ◽  
Cell Stage ◽  
Unequal Distribution ◽  
Fate Determinants ◽  
Cell Fate Determinants

Cell lineage determination during early embryogenesis has profound effects on adult animal development. Pre-patterning of embryos, such as that of Drosophila and Caenorhabditis elegans, is driven by asymmetrically localized maternal or zygotic factors, including mRNA species and RNA binding proteins. However, it is not clear how mammalian early embryogenesis is regulated and what the early cell fate determinants are. Here we show that, in mouse, mitochondrial ribosomal RNAs (mtrRNAs) are differentially distributed between 2-cell sister blastomeres. This distribution pattern is not related to the overall quantity or activity of mitochondria which appears equal between 2-cell sister blastomeres. Like in lower species, 16S mtrRNA is found to localize in the cytoplasm outside of mitochondria in mouse 2-cell embryos. Alterations of 16S mtrRNA levels in one of the 2-cell sister blastomere via microinjection of either sense or anti-sense RNAs drive its progeny into different cell lineages in blastocyst. These results indicate that mtrRNAs are differentially distributed among embryonic cells at the beginning of embryogenesis in mouse and they are functionally involved in the regulation of cell lineage allocations in blastocyst, suggesting an underlying molecular mechanism that regulates pre-implantation embryogenesis in mouse.

Promoting notochord fate and repressing muscle development in zebrafish axial mesoderm

Development ◽  
1998 ◽  
Vol 125 (8) ◽  
pp. 1397-1406 ◽  
Author(s):  
S.L. Amacher ◽  
C.B. Kimmel
Keyword(s):  
Cell Fate ◽  
Double Mutant ◽  
Muscle Development ◽  
Genetic Interaction ◽  
Embryonic Cells ◽  
Wild Type ◽  
Environmental Signals ◽  
Cell Fate Decisions ◽  
Muscle Genes ◽  
Midline Cells

Cell fate decisions in early embryonic cells are controlled by interactions among developmental regulatory genes. Zebrafish floating head mutants lack a notochord; instead, muscle forms under the neural tube. As shown previously, axial mesoderm in floating head mutant gastrulae fails to maintain expression of notochord genes and instead expresses muscle genes. Zebrafish spadetail mutant gastrulae have a nearly opposite phenotype; notochord markers are expressed in a wider domain than in wild-type embryos and muscle marker expression is absent. We examined whether these two phenotypes revealed an antagonistic genetic interaction by constructing the double mutant. Muscle does not form in the spadetail;floating head double mutant midline, indicating that spadetail function is required for floating head mutant axial mesoderm to transfate to muscle. Instead, the midline of spadetail;floating head double mutants is greatly restored compared to that of floating head mutants; the floor plate is almost complete and an anterior notochord develops. In addition, we find that floating head mutant cells can make both anterior and posterior notochord when transplanted into a wild-type host, showing that enviromental signals can override the predisposition of floating head mutant midline cells to make muscle. Taken together, these results suggest that repression of spadetail function by floating head is critical to promote notochord fate and prevent midline muscle development, and that cells can be recruited to the notochord by environmental signals.

scholarly journals IgH isotype-specific B cell receptor expression influences B cell fate

2017 ◽  
Vol 114 (40) ◽  
pp. E8411-E8420 ◽  
Author(s):  
Pei Tong ◽  
Alessandra Granato ◽  
Teng Zuo ◽  
Neha Chaudhary ◽  
Adam Zuiani ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Cell Fate ◽  
Rna Splicing ◽  
Memory Function ◽  
Cell Receptor ◽  
Receptor Expression ◽  
Wild Type ◽  
Cell Stage ◽  
Membrane Bound

Ig heavy chain (IgH) isotypes (e.g., IgM, IgG, and IgE) are generated as secreted/soluble antibodies (sIg) or as membrane-bound (mIg) B cell receptors (BCRs) through alternative RNA splicing. IgH isotype dictates soluble antibody function, but how mIg isotype influences B cell behavior is not well defined. We examined IgH isotype-specific BCR function by analyzing naturally switched B cells from wild-type mice, as well as by engineering polyclonal Ighγ1/γ1 and Ighε/ε mice, which initially produce IgG1 or IgE from their respective native genomic configurations. We found that B cells from wild-type mice, as well as Ighγ1/γ1 and Ighε/ε mice, produce transcripts that generate IgM, IgG1, and IgE in an alternative splice form bias hierarchy, regardless of cell stage. In this regard, we found that mIgμ > mIgγ1 > mIgε, and that these BCR expression differences influence respective developmental fitness. Restrained B cell development from Ighγ1/γ1 and Ighε/ε mice was proportional to sIg/mIg ratios and was rescued by enforced expression of the respective mIgs. In addition, artificially enhancing BCR signal strength permitted IgE+ memory B cells—which essentially do not exist under normal conditions—to provide long-lived memory function, suggesting that quantitative BCR signal weakness contributes to restraint of IgE B cell responses. Our results indicate that IgH isotype-specific mIg/BCR dosage may play a larger role in B cell fate than previously anticipated.

scholarly journals The genetic basis for the evolution of soma: mechanistic evidence for the co-option of a stress-induced gene into a developmental master regulator

2020 ◽  
Vol 287 (1940) ◽  
pp. 20201414
Author(s):  
Stephan G. König ◽  
Aurora M. Nedelcu
Keyword(s):  
Cell Fate ◽  
Stress Responses ◽  
Regulatory Gene ◽  
Somatic Cells ◽  
Cell Types ◽  
Volvox Carteri ◽  
Developmentally Regulated ◽  
Evolutionary Origins ◽  
Increased Sensitivity ◽  
Multicellular Organisms

In multicellular organisms with specialized cells, the most significant distinction among cell types is between reproductive (germ) cells and non-reproductive/somatic cells (soma). Although soma contributed to the marked increase in complexity of many multicellular lineages, little is known about its evolutionary origins. We have previously suggested that the evolution of genes responsible for the differentiation of somatic cells involved the co-option of life history trade-off genes that in unicellular organisms enhanced survival at a cost to immediate reproduction. In the multicellular green alga, Volvox carteri , cell fate is established early in development by the differential expression of a master regulatory gene known as regA . A closely related RegA -Like Sequence ( RLS1 ) is present in its single-celled relative, Chlamydomonas reinhardtii . RLS1 is expressed in response to stress, and we proposed that an environmentally induced RLS1 -like gene was co-opted into a developmental pathway in the lineage leading to V. carteri . However, the exact evolutionary scenario responsible for the postulated co-option event remains to be determined. Here, we show that in addition to being developmentally regulated, regA can also be induced by environmental cues, indicating that regA has maintained its ancestral regulation. We also found that the absence of a functional RegA protein confers increased sensitivity to stress, consistent with RegA having a direct or indirect role in stress responses. Overall, this study (i) provides mechanistic evidence for the co-option of an environmentally induced gene into a major developmental regulator, (ii) supports the view that major morphological innovations can evolve via regulatory changes and (iii) argues for the role of stress in the evolution of multicellular complexity.

scholarly journals KLU suppresses megasporocyte cell fate through SWR1-mediated activation of WRKY28 expression in Arabidopsis

2017 ◽  
Vol 115 (3) ◽  
pp. E526-E535 ◽  
Author(s):  
Lihua Zhao ◽  
Hanyang Cai ◽  
Zhenxia Su ◽  
Lulu Wang ◽  
Xinyu Huang ◽  
...  
Keyword(s):  
Single Cell ◽  
Cell Fate ◽  
Chromatin Remodeling ◽  
Molecular Mechanisms ◽  
Germ Line ◽  
Somatic Cells ◽  
Cell Specification ◽  
Germ Line Cell ◽  
P450 Gene ◽  
Female Germ Line

Germ-line specification is essential for sexual reproduction. In the ovules of most flowering plants, only a single hypodermal cell enlarges and differentiates into a megaspore mother cell (MMC), the founder cell of the female germ-line lineage. The molecular mechanisms restricting MMC specification to a single cell remain elusive. We show that the Arabidopsis transcription factor WRKY28 is exclusively expressed in hypodermal somatic cells surrounding the MMC and is required to repress these cells from acquiring MMC-like cell identity. In this process, the SWR1 chromatin remodeling complex mediates the incorporation of the histone variant H2A.Z at the WRKY28 locus. Moreover, the cytochrome P450 gene KLU, expressed in inner integument primordia, non–cell-autonomously promotes WRKY28 expression through H2A.Z deposition at WRKY28. Taken together, our findings show how somatic cells in ovule primordia cooperatively use chromatin remodeling to restrict germ-line cell specification to a single cell.

The program for cellular differentiation in Volvox carteri as revealed by molecular analysis of development in a gonidialess/somatic regenerator mutant

Development ◽  
1991 ◽  
Vol 112 (2) ◽  
pp. 571-580 ◽  
Author(s):  
L.W. Tam ◽  
D.L. Kirk
Keyword(s):  
Initial Period ◽  
Molecular Genetic ◽  
Somatic Cells ◽  
Wild Type ◽  
Volvox Carteri ◽  
Distinct Cell ◽  
Cell Type Specific ◽  
Development Levels ◽  
Type V ◽  
Mutant Cells

Development of a ‘gonidialess’/‘somatic regenerator’ double mutant of Volvox carteri was analyzed with a number of cell-type-specific cDNA probes that had been identified in a previous study. Whereas in wild-type strains somatic cells and gonidia (asexual reproductive cells) constitute two distinct cell lineages, in this mutant all cells first differentiate as somatic cells and then redifferentiate as gonidia. During the initial period of somatic differentiation, we found that both gonidial and ‘early’ somatic transcripts were accumulated in the mutant, consistent with the idea that it is the regA gene product (which is defective in this mutant) that normally acts to suppress gonidial gene expression in somatic cells. Later in development, levels of early somatic transcripts fell abruptly, levels of the late somatic transcripts remained extremely low, and levels of gonidial transcripts rose as the cells redifferentiated. Thus it appears that in the mutant cells the gonidial program of development takes over and somatic differentiation is aborted before the stage at which late somatic genes are normally activated. These results provide molecular genetic support for a model which postulates that three types of genes (including the two that are defective in the strain studied here) are crucial for converting the sequential program of differentiation seen in more primitive volvocalean algae to the dichotomous program of germ-soma differentiation that occurs in wild-type V. carteri.

scholarly journals Two maternal genes, apx-1 and pie-1, are required to distinguish the fates of equivalent blastomeres in the early Caenorhabditis elegans embryo

Development ◽  
1994 ◽  
Vol 120 (8) ◽  
pp. 2305-2315 ◽  
Author(s):  
S.E. Mango ◽  
C.J. Thorpe ◽  
P.R. Martin ◽  
S.H. Chamberlain ◽  
B. Bowerman
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Fate ◽  
Cell Types ◽  
Developmental State ◽  
Signalling Pathway ◽  
Wild Type ◽  
Cell Stage ◽  
Developmental Potential ◽  
Recessive Mutations ◽  
Unique Cell

In a 4-cell Caenorhabditis elegans embryo, two sister blastomeres called ABa and ABp are born with equivalent developmental potential, but eventually produce distinct patterns of cell fate. The different fates of ABa and ABp are specified at least in part by inductive interactions with neighboring blastomeres. Previous studies indicate that, at the 4-cell stage, a signal from the posterior-most blastomere, P2, is required for ABp to produce at least one of its unique cell types. This P2/ABp interaction depends on glp-1, a putative receptor for intercellular interactions. To investigate this early induction further, we isolated mutants in which ABp developed abnormally. We describe the effects of recessive mutations in apx-1, a maternal gene that appears to be required for P2 to signal ABp. In embryos from mothers homozygous for mutations in apx-1 (apx-1 embryos), ABp fails to produce its characteristic cell types. Instead, ABp from apx-1 embryos develops more like its sister ABa: it produces ABa-like pharyngeal cells and it recapitulates ABa-like cell lineages. Because mutations in apx-1 affect the development of only the ABp blastomere, we suggest that the wild-type gene encodes a component of the P2/ABp signalling pathway. To explain the observation that ABp in apx-1 embryos adopts an ABa-like fate, we propose a model in which the P2 signal is required to break the initial equivalence of ABa and ABp. We performed two independent tests of this model. First, we examined ABp development in pie-1 mutant embryos, in which P2 adopts the identity of another blastomere. We find that, in pie-1 embryos, APp fails to produce its characteristic cell types and instead adopts a fate similar to that of ABa. We conclude that the changed identity of P2 in pie-1 embryos prevents the P2/ABp interaction. As a second test, we examined ABp development in wild-type embryos after physically removing P2. These operated embryos produce extra pharyngeal cells, consistent with out proposal that a signal from P2 breaks the initially equivalent developmental state of ABa and ABp. We discuss the possibility that apx-1 acts as a ligand in this glp-1-dependent signalling pathway.

Metabolic Regulation of Hippocampal Neuronal Development and Its Inhibition After Irradiation

2021 ◽  
Vol 80 (5) ◽  
pp. 467-475
Author(s):  
Yu-Qing Li ◽  
C Shun Wong
Keyword(s):  
Cell Fate ◽  
Metabolic Regulation ◽  
Energy Homeostasis ◽  
Neuronal Development ◽  
Adenosine Monophosphate ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Wild Type ◽  
Newborn Neuron ◽  
Negative Effect

Abstract 5′-Adenosine monophosphate-activated protein kinase (AMPK), a key regulator of cellular energy homeostasis, plays a role in cell fate determination. Whether AMPK regulates hippocampal neuronal development remains unclear. Hippocampal neurogenesis is abrogated after DNA damage. Here, we asked whether AMPK regulates adult hippocampal neurogenesis and its inhibition following irradiation. Adult Cre-lox mice deficient in AMPK in brain, and wild-type mice were used in a birth-dating study using bromodeoxyuridine to evaluate hippocampal neurogenesis. There was no evidence of AMPK or phospho-AMPK immunoreactivity in hippocampus. Increase in p-AMPK but not AMPK expression was observed in granule neurons and subgranular neuroprogenitor cells (NPCs) in the dentate gyrus within 24 hours and persisted up to 9 weeks after irradiation. AMPK deficiency in Cre-lox mice did not alter neuroblast and newborn neuron numbers but resulted in decreased newborn and proliferating NPCs. Inhibition of neurogenesis was observed after irradiation regardless of genotypes. In Cre-lox mice, there was further loss of newborn early NPCs and neuroblasts but not newborn neurons after irradiation compared with wild-type mice. These results are consistent with differential negative effect of AMPK on hippocampal neuronal development and its inhibition after irradiation.

scholarly journals cot1: A Regulator of Arabidopsis Trichome Initiation

Genetics ◽  
1998 ◽  
Vol 149 (2) ◽  
pp. 565-577
Author(s):  
Daniel B Szymanski ◽  
Daniel A Klis ◽  
John C Larkin ◽  
M David Marks
Keyword(s):  
Cell Fate ◽  
Gene Dosage ◽  
Signal Transduction Pathway ◽  
Spatial Arrangement ◽  
Complex Signal ◽  
Chromosome 2 ◽  
Wild Type ◽  
Trichome Formation ◽  
In The Wild ◽  
Leaf Trichome

Abstract In Arabidopsis, the timing and spatial arrangement of trichome initiation is tightly regulated and requires the activity of the GLABROUS1 (GL1) gene. The COTYLEDON TRICHOME 1 (COT1) gene affects trichome initiation during late stages of leaf development and is described in this article. In the wild-type background, cot1 has no observable effect on trichome initiation. GL1 overexpression in wild-type plants leads to a modest number of ectopic trichomes and to a decrease in trichome number on the adaxial leaf surface. The cot1 mutation enhances GL1-overexpression-dependent ectopic trichome formation and also induces increased leaf trichome initiation. The expressivity of the cot1 phenotype is sensitive to cot1 and 35S::GL1 gene dosage, and the most severe phenotypes are observed when cot1 and 35S::GL1 are homozygous. The COT1 locus is located on chromosome 2 15.3 cM north of er. Analysis of the interaction between cot1, try, and 35S::GL1 suggests that COT1 is part of a complex signal transduction pathway that regulates GL1-dependent adoption of the trichome cell fate.

Peripheral T-cell lymphomas unspecified presenting in the skin: analysis of prognostic factors in a group of 82 patients

Blood ◽  
2003 ◽  
Vol 102 (6) ◽  
pp. 2213-2219 ◽  
Author(s):  
Marcel W. Bekkenk ◽  
Maarten H. Vermeer ◽  
Patty M. Jansen ◽  
Ariënne M. W. van Marion ◽  
Marijke R. Canninga-van Dijk ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Size ◽  
Cell Lymphoma ◽  
Large Cell ◽  
Skin Lesions ◽  
T Cell Lymphoma ◽  
Peripheral T Cell Lymphoma ◽  
T Cell Lymphomas ◽  
Nor Phenotype ◽  
Peripheral T Cell Lymphomas

Abstract In the present study the clinicopathologic and immunophenotypic features of 82 patients with a CD30– peripheral T-cell lymphoma, unspecified, presenting in the skin were evaluated. The purpose of this study was to find out whether subdivision of these lymphomas on the basis of cell size, phenotype, or presentation with only skin lesions is clinically relevant. The study group included 46 primary cutaneous CD30– large cell lymphomas and 17 small/medium-sized T-cell lymphomas as well as 17 peripheral T-cell lymphomas with both skin and extracutaneous disease at the time of diagnosis. Patients with primary cutaneous small- or medium-sized T-cell lymphomas had a significantly better prognosis (5-year-overall survival, 45%) than patients with primary cutaneous CD30– large T-cell lymphomas (12%) and patients presenting with concurrent extracutaneous disease (12%). The favorable prognosis in this group with primary cutaneous small- or medium-sized T-cell lymphomas was particularly found in patients presenting with localized skin lesions expressing a CD3+CD4+CD8– phenotype. In the primary cutaneous T-cell lymphoma (CTCL) group and in the concurrent group, neither extent of skin lesions nor phenotype had any effect on survival. Our results indicate that peripheral T-cell lymphomas, unspecified, presenting in the skin have an unfavorable prognosis, irrespective of the presence or absence of extracutaneous disease at the time of diagnosis, cell size, and expression of a CD4+ or CD8+ phenotype. The only exception was a group of primary cutaneous small- or medium-sized pleomorphic CTCLs with a CD3+CD4+CD8– phenotype and presenting with localized skin lesions.

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