The maternal par genes and the segregation of cell fate specification activities in early Caenorhabditis elegans embryos

Development ◽  
1997 ◽  
Vol 124 (19) ◽  
pp. 3815-3826 ◽  
Author(s):  
B. Bowerman ◽  
M.K. Ingram ◽  
C.P. Hunter
Keyword(s):  
Cell Fate ◽  
Expression Patterns ◽  
Control Cell ◽  
Gene Products ◽  
Cell Fate Specification ◽  
Loss Of Function ◽  
C Elegans ◽  
Embryonic Polarity ◽  
Early Embryos ◽  
Anterior Posterior

After fertilization in C. elegans, activities encoded by the maternally expressed par genes appear to establish cellular and embryonic polarity. Loss-of-function mutations in the par genes disrupt anterior-posterior (a-p) asymmetries in early embryos and result in highly abnormal patterns of cell fate. Little is known about how the early asymmetry defects are related to the cell fate patterning defects in par mutant embryos, or about how the par gene products affect the localization and activities of developmental regulators known to specify the cell fate patterns made by individual blastomeres. Examples of such regulators of blastomere identity include the maternal proteins MEX-3 and GLP-1, expressed at high levels anteriorly, and SKN-1 and PAL-1, expressed at high levels posteriorly in early embryos. To better define par gene functions, we examined the expression patterns of MEX-3, PAL-1 and SKN-1, and we analyzed mex-3, pal-1, skn-1 and glp-1 activities in par mutant embryos. We have found that mutational inactivation of each par gene results in a unique phenotype, but in no case do we observe a complete loss of a-p asymmetry. We conclude that no one par gene is required for all a-p asymmetry and we suggest that, in some cases, the par genes act independently of each other to control cell fate patterning and polarity. Finally, we discuss the implications of our findings for understanding how the initial establishment of polarity in the zygote by the par gene products leads to the proper localization of more specifically acting regulators of blastomere identity.

scholarly journals Spatial and temporal patterns of lin-12 expression during C. elegans hermaphrodite development.

Genetics ◽  
1995 ◽  
Vol 141 (2) ◽  
pp. 513-526
Author(s):  
H A Wilkinson ◽  
I Greenwald
Keyword(s):  
Cell Fate ◽  
Reporter Gene ◽  
Control Cell ◽  
Cell Fate Specification ◽  
Lacz Reporter ◽  
Spatial And Temporal Patterns ◽  
Lacz Reporter Gene ◽  
Vulval Development ◽  
C Elegans ◽  
A Cell

Abstract The lin-12 gene encodes a receptor that mediates certain cell-cell interactions during Caenorhabditis elegans development. We have examined the expression of a lin-12::lacZ reporter gene in individual cells during the development of C. elegans hermaphrodites. lin-12::lacZ is expressed in a discrete spatial and temporal pattern during development and teh lin-12::lacZ reporter gene will provide a useful marker for other studies, particularly of somatic gonadal and vulval development. In general, the cells that express lin-12:: lacZ correspond to cells whose fates are known to be altered in lin-12 mutants implying that restriction of lin-12 expression may be an important regulatory mechanism; the exceptions to this statement may reveal the cellular defects that underlie aspects of the lin-12 phenotype that have not been previously explained. For decisions that are not naturally variable, lin-12::lacZ expression does not appear to change before or upon commitment to a cell fate implying that in these cases postranscriptional regulation of lin-12 activity may control cell fate specification.

scholarly journals Notch signaling coordinates ommatidial rotation in the Drosophila eye via transcriptional regulation of the EGF-Receptor ligand Argos

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Yildiz Koca ◽  
Benjamin E. Housden ◽  
William J. Gault ◽  
Sarah J. Bray ◽  
Marek Mlodzik
Keyword(s):  
Notch Signaling ◽  
Cell Fate ◽  
Planar Cell Polarity ◽  
Egf Receptor ◽  
Control Cell ◽  
Loss Of Function ◽  
Egfr Signaling ◽  
Specific Expression ◽  
Egfr Signaling Pathway ◽  
Ommatidial Rotation

AbstractIn all metazoans, a small number of evolutionarily conserved signaling pathways are reiteratively used during development to orchestrate critical patterning and morphogenetic processes. Among these, Notch (N) signaling is essential for most aspects of tissue patterning where it mediates the communication between adjacent cells to control cell fate specification. In Drosophila, Notch signaling is required for several features of eye development, including the R3/R4 cell fate choice and R7 specification. Here we show that hypomorphic alleles of Notch, belonging to the Nfacet class, reveal a novel phenotype: while photoreceptor specification in the mutant ommatidia is largely normal, defects are observed in ommatidial rotation (OR), a planar cell polarity (PCP)-mediated cell motility process. We demonstrate that during OR Notch signaling is specifically required in the R4 photoreceptor to upregulate the transcription of argos (aos), an inhibitory ligand to the epidermal growth factor receptor (EGFR), to fine-tune the activity of EGFR signaling. Consistently, the loss-of-function defects of Nfacet alleles and EGFR-signaling pathway mutants are largely indistinguishable. A Notch-regulated aos enhancer confers R4 specific expression arguing that aos is directly regulated by Notch signaling in this context via Su(H)-Mam-dependent transcription.

scholarly journals pop-1/TCF, ref-2/ZIC and T-box factors regulate the development of anterior cells in the C. elegans embryo

2021 ◽  
Author(s):  
Jonathan D Rumley ◽  
Elicia A Preston ◽  
Dylan Cook ◽  
Felicia L Peng ◽  
Amanda L Zacharias ◽  
...  
Keyword(s):  
Wnt Pathway ◽  
Expression Patterns ◽  
Specific Expression ◽  
T Box ◽  
Animal Development ◽  
C Elegans ◽  
The Many ◽  
Necessary And Sufficient ◽  
Cell Division Timing ◽  
Anterior Posterior

Patterning of the anterior-posterior axis is fundamental to animal development. The Wnt pathway plays a major role in this process by activating the expression of posterior genes in animals from worms to humans. This observation raises the question of whether the Wnt pathway or other regulators control the expression of the many anterior-expressed genes. We found that the expression of five anterior-specific genes in Caenorhabditis elegans embryos depends on the Wnt pathway effectors pop-1/TCF and sys-1/β-catenin. We focused further on one of these anterior genes, ref-2/ZIC, a conserved transcription factor expressed in multiple anterior lineages. Live imaging of ref-2 mutant embryos identified defects in cell division timing and position in anterior lineages. Cis-regulatory dissection identified three ref-2 transcriptional enhancers, one of which is necessary and sufficient for anterior-specific expression. This enhancer is activated by the T-box transcription factors TBX-37 and TBX-38, and surprisingly, concatemerized TBX-37/38 binding sites are sufficient to drive anterior-biased expression alone, despite the broad expression of TBX-37 and TBX-38. Taken together, our results highlight the diverse mechanisms used to regulate anterior expression patterns in the embryo.

scholarly journals CFP-1 interacts with HDAC1/2 complexes inC. elegansdevelopment

2018 ◽  
Author(s):  
Bharat Pokhrel ◽  
Yannic Chen ◽  
Jonathan Joseph Biro
Keyword(s):  
Cell Fate ◽  
Embryonic Stem ◽  
Stem Cell Differentiation ◽  
Embryonic Stem Cell Differentiation ◽  
Dependent Manner ◽  
Cell Fate Specification ◽  
C Elegans ◽  
Evolutionarily Conserved ◽  
Epigenetic Regulator ◽  
Inducible Genes

AbstractCFP-1 (CXXC finger binding protein 1) is an evolutionarily conserved protein that binds to non-methylated CpG-rich promoters in humans andC. elegans. This conserved epigenetic regulator is a part of the COMPASS complex that contains the H3K4me3 methyltransferase SET1 in mammals and SET-2 inC. elegans. Previous studies have indicated the importance ofcfp-1in embryonic stem cell differentiation and cell fate specification. However, neither the function nor the mechanism of action ofcfp-1is well understood at the organismal level. To further investigate the function of CFP-1, we have characterisedC. elegansCOMPASS mutantscfp-1(tm6369)andset-2(bn129). We found that bothcfp-1andset-2play an important role in the regulation of fertility and development of the organism. Furthermore, we found that bothcfp-1andset-2are required for H3K4 trimethylation and play a repressive role in the expression of heat shock and salt-inducible genes. Interestingly, we found thatcfp-1but notset-2genetically interacts with Histone Deacetylase (HDAC1/2) complexes to regulate fertility, suggesting a function of CFP-1 outside of the COMPASS complex. Additionally we found thatcfp-1andset-2acts on a separate pathways to regulate fertility and development ofC. elegans. Our results suggest that CFP-1 genetically interacts with HDAC1/2 complexes to regulate fertility, independent of its function within COMPASS complex. We propose that CFP-1 could cooperate with COMPASS complex and/or HDAC1/2 in a context dependent manner.

scholarly journals Differential regulation of gastrulation and neuroectodermal gene expression by Snail in the Drosophila embryo

Development ◽  
1997 ◽  
Vol 124 (19) ◽  
pp. 3683-3691 ◽  
Author(s):  
K. Hemavathy ◽  
X. Meng ◽  
Y.T. Ip
Keyword(s):  
Cell Fate ◽  
Target Genes ◽  
Expression Patterns ◽  
Cell Movement ◽  
Drosophila Embryo ◽  
Intermediate Phenotype ◽  
Gene Products ◽  
Mesodermal Cell ◽  
Possible Cause ◽  
Mesodermal Lineage

The initiation of mesoderm differentiation in the Drosophila embryo requires the gene products of twist and snail. In either mutant, the ventral cell invagination during gastrulation is blocked and no mesoderm-derived tissue is formed. One of the functions of Snail is to repress neuroectodermal genes and restrict their expressions to the lateral regions. The derepression of the neuroectodermal genes into the ventral region in snail mutant is a possible cause of defects in gastrulation and in mesoderm differentiation. To investigate such possibility, we analysed a series of snail mutant alleles. We found that different neuroectodermal genes respond differently in various snail mutant background. Due to the differential response of target genes, one of the mutant alleles, V2, that has reduced Snail function showed an intermediate phenotype. In V2 embryos, neuroectodermal genes, such as single-minded and rhomboid, are derepressed while ventral invagination proceeds normally. However, the differentiation of these invaginated cells into mesodermal lineage is disrupted. The results suggest that the establishment of mesodermal cell fate requires the proper restriction of neuroectodermal genes, while the ventral cell movement is independent of the expression patterns of these genes. Together with the data showing that the expression of some ventral genes disappear in snail mutants, we propose that Snail may repress or activate another set of target genes that are required specifically for gastrulation.

Specification of anterior-posterior differences within the AB lineage in the C. elegans embryo: a polarising induction

Development ◽  
1995 ◽  
Vol 121 (5) ◽  
pp. 1559-1568 ◽  
Author(s):  
H. Hutter ◽  
R. Schnabel
Keyword(s):  
Cell Fate ◽  
Tissue Type ◽  
Cell Stage ◽  
Anterior Portion ◽  
Developmental Potential ◽  
C Elegans ◽  
The Third ◽  
Inductive Signal ◽  
Anterior Posterior ◽  
Lineage Analysis

In a C. elegans embryo the third cleavages of descendants of the anterior blastomere AB of the 2-cell stage create pairs of blastomeres that develop differently. By laser ablation experiments we show that the fates of all the posterior daughters of this division depend on an induction occurring three cleavages before these blastomeres are born. The time of induction precludes a direct effect on cell fate. Alternatively, we suggest that the induction creates a heritable cell polarity which is propagated through several divisions. We suggest a model to demonstrate how a signal could be propagated through several rounds of cell division. An important implication of our observations is that this early induction acts to specify blastomere identity, not tissue type. A detailed lineage analysis revealed that altering the inductive signal alters complex lineage patterns as a whole. The induction described here, together with two inductions described previously can be used to illustrate how the anterior portion of the C. elegans embryo can be successively subdivided into blastomeres with unique developmental potential.

A predicted membrane protein, TRA-2A, directs hermaphrodite development in Caenorhabditis elegans

Development ◽  
1995 ◽  
Vol 121 (9) ◽  
pp. 2995-3004 ◽  
Author(s):  
P.E. Kuwabara ◽  
J. Kimble
Keyword(s):  
Heat Shock ◽  
Membrane Protein ◽  
Cell Fate ◽  
Loss Of Function ◽  
Heat Shock Promoter ◽  
Somatic Development ◽  
C Elegans ◽  
Cellular Domain ◽  
Carboxy Terminal ◽  
Necessary And Sufficient

The nematode C. elegans naturally develops as either an XO male or XX hermaphrodite. The sex-determining gene, tra-2, promotes hermaphrodite development in XX animals. This gene encodes a predicted membrane protein, named TRA-2A, which has been proposed to provide the primary feminising activity of the tra-2 locus. Here, we show that transgenic TRA-2A driven from a heat shock promoter can fully feminise the somatic tissues of XX tra-2 loss-of-function mutants, which would otherwise develop as male. TRA-2A is thus likely to provide a component of the tra-2 locus that is both necessary and sufficient to promote female somatic development. Transgenic TRA-2A driven by the heat shock promoter can also transform XO animals from male to self-fertile hermaphrodite. This result establishes the role of tra-2 as a developmental switch that controls somatic sexual cell fate. We show that a carboxy-terminal region of TRA-2A, predicted to be intra-cellular, can partially feminise XX tra-2 loss-of-function mutants and XO tra-2(+) males. We suggest that this intra-cellular domain of TRA-2A promotes hermaphrodite development by negatively regulating the FEM proteins.

The C. elegans NeuroD homolog cnd-1 functions in multiple aspects of motor neuron fate specification

Development ◽  
2000 ◽  
Vol 127 (19) ◽  
pp. 4239-4252 ◽  
Author(s):  
S. Hallam ◽  
E. Singer ◽  
D. Waring ◽  
Y. Jin
Keyword(s):  
Motor Neuron ◽  
Motor Neurons ◽  
Expression Patterns ◽  
Loss Of Function ◽  
Variable Expression ◽  
C Elegans ◽  
Helix Loop Helix ◽  
Ventral Cord ◽  
Bhlh Proteins ◽  
Neuronal Type

The basic helix-loop-helix transcription factor NeuroD (Neurod1) has been implicated in neuronal fate determination, differentiation and survival. Here we report the expression and functional analysis of cnd-1, a C. elegans NeuroD homolog. cnd-1 expression was first detected in neuroblasts of the AB lineage in 14 cell embryos and maintained in many neuronal descendants of the AB lineage during embryogenesis, diminishing in most terminally differentiated neurons prior to hatching. Specifically, cnd-1 reporter genes were expressed in the precursors of the embryonic ventral cord motor neurons and their progeny. A loss-of-function mutant, cnd-1(ju29), exhibited multiple defects in the ventral cord motor neurons. First, the number of motor neurons was reduced, possibly caused by the premature withdrawal of the precursors from mitotic cycles. Second, the strict correlation between the fate of a motor neuron with respect to its lineage and position in the ventral cord was disrupted, as manifested by the variable expression pattern of motor neuron fate specific markers. Third, motor neurons also exhibited defects in terminal differentiation characteristics including axonal morphology and synaptic connectivity. Finally, the expression patterns of three neuronal type-specific transcription factors, unc-3, unc-4 and unc-30, were altered. Our data suggest that cnd-1 may specify the identity of ventral cord motor neurons both by maintaining the mitotic competence of their precursors and by modulating the expression of neuronal type-specific determination factors. cnd-1 appears to have combined the functions of several vertebrate neurogenic bHLH proteins and may represent an ancestral form of this protein family.

Genes necessary for C. elegans cell and growth cone migrations

Development ◽  
1997 ◽  
Vol 124 (9) ◽  
pp. 1831-1843 ◽  
Author(s):  
W.C. Forrester ◽  
G. Garriga
Keyword(s):  
Cell Fate ◽  
Single Gene ◽  
Growth Cones ◽  
Cell Fate Specification ◽  
Fate Specification ◽  
C Elegans ◽  
Final Destination ◽  
Multiple Cell

The migrations of cells and growth cones contribute to form and pattern during metazoan development. To study the mechanisms that regulate cell motility, we have screened for C. elegans mutants defective in the posteriorly directed migrations of the canal-associated neurons (CANs). Here we describe 14 genes necessary for CAN cell migration. Our characterization of the mutants has led to three conclusions. First, the mutations define three gene classes: genes necessary for cell fate specification, genes necessary for multiple cell migrations and a single gene necessary for final positioning of migrating cells. Second, cell interactions between the CAN and HSN, a neuron that migrates anteriorly to a position adjacent to the CAN, control the final destination of the HSN cell body. Third, C. elegans larval development requires the CANs. In the absence of CAN function, larvae arrest development, with excess fluid accumulating in their pseudocoeloms. This phenotype may reflect a role of the CANs in osmoregulation.

scholarly journals Calcineurin homologous proteins regulate the membrane localization and activity of sodium/proton exchangers in C. elegans

2016 ◽  
Vol 310 (3) ◽  
pp. C233-C242 ◽  
Author(s):  
Erik Allman ◽  
Qian Wang ◽  
Rachel L. Walker ◽  
Molly Austen ◽  
Maureen A. Peters ◽  
...  
Keyword(s):  
Genetic Model ◽  
Expression Patterns ◽  
Critical Role ◽  
Model Organism ◽  
Loss Of Function ◽  
Homologous Proteins ◽  
Relative Significance ◽  
C Elegans ◽  
Fluorescent Tags

Calcineurin B homologous proteins (CHP) are N-myristoylated, EF-hand Ca2+-binding proteins that bind to and regulate Na+/H+ exchangers, which occurs through a variety of mechanisms whose relative significance is incompletely understood. Like mammals, Caenorhabditis elegans has three CHP paralogs, but unlike mammals, worms can survive CHP loss-of-function. However, mutants for the CHP ortholog PBO-1 are unfit, and PBO-1 has been shown to be required for proton signaling by the basolateral Na+/H+ exchanger NHX-7 and for proton-coupled intestinal nutrient uptake by the apical Na+/H+ exchanger NHX-2. Here, we have used this genetic model organism to interrogate PBO-1's mechanism of action. Using fluorescent tags to monitor Na+/H+ exchanger trafficking and localization, we found that loss of either PBO-1 binding or activity caused NHX-7 to accumulate in late endosomes/lysosomes. In contrast, NHX-2 was stabilized at the apical membrane by a nonfunctional PBO-1 protein and was only internalized following its complete loss. Additionally, two pbo-1 paralogs were identified, and their expression patterns were analyzed. One of these contributed to the function of the excretory cell, which acts like a kidney in worms, establishing an alternative model for testing the role of this protein in membrane transporter trafficking and regulation. These results lead us to conclude that the role of CHP in Na+/H+ exchanger regulation differs between apical and basolateral transporters. This further emphasizes the importance of proper targeting of Na+/H+ exchangers and the critical role of CHP family proteins in this process.

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