Posterior Daughter Cell Research Articles

The identity of Centrodinium elongatum, type species of the dinoflagellate genus Centrodinium (Dinophyceae), and a review on the synonymy of allied species.

The planktonic dinoflagellate genus Centrodinium has been understudied, with the type species C. elongatum remaining undocumented since the original description. Here, we report C. elongatum isolated from Mazatlán, Mexican Pacific. In the chains, the posterior daughter cell with an incomplete apical horn shows the morphology of C. elongatum, while the anterior daughter cell with complete epitheca corresponds to C. pulchrum. For the first time, a species of Centrodinium sensu stricto (highly laterally flattened species with horns) was cultured. An unarmored life stage, known as Murrayella ovalis, derived from the spheroplast after ecdysis. In the rDNA molecular phylogenies, C. elongatum (=C. pulchrum) nested as basal to morphologically similar species (C. eminens and C. intermedium) and as a sister group of a former Murrayella species, C. punctatum. C. elongatum differs from C. eminens and C. intermedium in the chain formation, second apical (2') plate not being divided, horns with coarse poroid ornamentation, and missing prominent distal spinules. The taxonomy of Centrodinium sensu stricto is revised, with a discussion in the identities of C. complanatum, C. eminens, and C. maximum. The name C. deflexum is restored as a senior synonym of C. intermedium and C. ovale.

PLK-1 regulates MEX-1 polarization in the C. elegans zygote.

The one-cell C. elegans embryo undergoes an asymmetric cell division during which germline factors such as the RNA-binding proteins POS-1 and MEX-1 segregate to the posterior cytoplasm, leading to their asymmetric inheritance to the posterior germline daughter cell. Previous studies found that the RNA-binding protein MEX-5 recruits polo-like kinase PLK-1 to the anterior cytoplasm where PLK-1 inhibits the retention of its substrate POS-1, leading to POS-1 segregation to the posterior. In this study, we tested whether PLK-1 similarly regulates MEX-1 polarization. We find that both the retention of MEX-1 in the anterior and the segregation of MEX-1 to the posterior depend on PLK kinase activity and on the interaction between MEX-5 and PLK-1. Human PLK1 directly phosphorylates recombinant MEX-1 on 9 predicted PLK-1 sites in vitro, four of which were identified in previous phosphoproteomic analysis of C. elegans embryos. The introduction of alanine substitutions at these four PLK-1 phosphorylation sites (MEX-1(4A)) significantly weakened the inhibition of MEX-1 retention in the anterior, thereby weakening MEX-1 segregation to the posterior. In contrast, mutation of a predicted CDK1 phosphorylation site had no effect on MEX-1 retention or on MEX-1 segregation. MEX-1(4A) mutants are viable and fertile but display significant sterility and fecundity defects at elevated temperatures. Taken together with our previous findings, these findings suggest PLK-1 phosphorylation drives both MEX-1 and POS-1 polarization during the asymmetric division of the zygote.

The complete cell lineage and MAPK- and Otx-dependent specification of the dopaminergic cells in the Ciona brain.

The Ciona larva has served as a unique model for understanding the development of dopaminergic cells at single-cell resolution owing to the exceptionally small number of neurons in its brain and its fixed cell lineage during embryogenesis. A recent study suggested that the transcription factors Fer2 and Meis directly regulate the dopamine synthesis genes in Ciona, but the dopaminergic cell lineage and the gene regulatory networks that control the development of dopaminergic cells have not been fully elucidated. Here, we reveal that the dopaminergic cells in Ciona are derived from a bilateral pair of cells called a9.37 cells at the center of the neural plate. The a9.37 cells divide along the anterior-posterior axis, and all of the descendants of the posterior daughter cells differentiate into the dopaminergic cells. We show that the MAPK pathway and the transcription factor Otx are required for the expression of Fer2 in the dopaminergic cell lineage. Our findings establish the cellular and molecular framework for fully understanding the commitment to dopaminergic cells in the simple chordate brain.

The first steps in the life of a worm: Themes and variations in asymmetric division in C. elegans and other nematodes.

Starting with Boveri in the 1870s, microscopic investigation of early embryogenesis in a broad swath of nematode species revealed the central role of asymmetric cell division in embryonic axis specification, blastomere positioning, and cell fate specification. Notably, across the class Chromadorea, a conserved theme emerges-asymmetry is first established in the zygote and specifies its asymmetric division, giving rise to an anterior somatic daughter cell and a posterior germline daughter cell. Beginning in the 1980s, the emergence of Caenorhabditis elegans as a model organism saw the advent of genetic tools that enabled rapid progress in our understanding of the molecular mechanisms underlying asymmetric division, in many cases defining key paradigms that turn out to regulate asymmetric division in a wide range of systems. Yet, the consequence of this focus on C. elegans came at the expense of exploring the extant diversity of developmental variation exhibited across nematode species. Given the resurgent interest in evolutionary studies facilitated in part by new tools, here we revisit the diversity in this asymmetric first division, juxtaposing molecular insight into mechanisms of symmetry-breaking, spindle positioning and fate specification, with a consideration of plasticity and variability within and between species. In the process, we hope to highlight questions of evolutionary forces and molecular variation that may have shaped the extant diversity of developmental mechanisms observed across Nematoda.

Two Antagonistic Hippo Signaling Circuits Set the Division Plane at the Medial Position in the Ciliate Tetrahymena.

In a single cell, ciliates maintain a complex pattern of cortical organelles that are arranged along the anteroposterior and circumferential axes. The underlying molecular mechanisms of intracellular pattern formation in ciliates are largely unknown. Ciliates divide by tandem duplication, a process that remodels the parental cell into two daughters aligned head-to-tail. In the elo1-1 mutant of Tetrahymena thermophila, the segmentation boundary/division plane forms too close to the posterior end of the parental cell, producing a large anterior and a small posterior daughter cell, respectively. We show that ELO1 encodes a Lats/NDR kinase that marks the posterior segment of the cell cortex, where the division plane does not form in the wild-type. Elo1 acts independently of CdaI, a Hippo/Mst kinase that marks the anterior half of the parental cell, and whose loss shifts the division plane anteriorly. We propose that, in Tetrahymena, two antagonistic Hippo circuits focus the segmentation boundary/division plane at the equatorial position, by excluding divisional morphogenesis from the cortical areas that are too close to cell ends.

The Hippo Pathway Maintains the Equatorial Division Plane in the Ciliate Tetrahymena.

The mechanisms that govern pattern formation within the cell are poorly understood. Ciliates carry on their surface an elaborate pattern of cortical organelles that are arranged along the anteroposterior and circumferential axes by largely unknown mechanisms. Ciliates divide by tandem duplication: the cortex of the predivision cell is remodeled into two similarly sized and complete daughters. In the conditional cdaI-1 mutant of Tetrahymena thermophila, the division plane migrates from its initially correct equatorial position toward the cell's anterior, resulting in unequal cell division, and defects in nuclear divisions and cytokinesis. We used comparative whole genome sequencing to identify the cause of cdaI-1 as a mutation in a Hippo/Mst kinase. CdaI is a cortical protein with a cell cycle-dependent, highly polarized localization. Early in cell division, CdaI marks the anterior half of the cell, and later concentrates at the posterior end of the emerging anterior daughter. Despite the strong association of CdaI with the new posterior cell end, the cdaI-1 mutation does not affect the patterning of the new posterior cortical organelles. We conclude that, in Tetrahymena, the Hippo pathway maintains an equatorial position of the fission zone, and, by this activity, specifies the relative dimensions of the anterior and posterior daughter cell.

Ephrin-mediated restriction of ERK1/2 activity delimits the number of pigment cells in the Ciona CNS

Recent evidence suggests that ascidian pigment cells are related to neural crest-derived melanocytes of vertebrates. Using live-imaging, we determine a revised cell lineage of the pigment cells in Ciona intestinalis embryos. The neural precursors undergo successive rounds of anterior–posterior (A–P) oriented cell divisions, starting at the blastula 64-cell stage. A previously unrecognized fourth A–P oriented cell division in the pigment cell lineage leads to the generation of the post-mitotic pigment cell precursors. We provide evidence that MEK/ERK signals are required for pigment cell specification until approximately 30min after the final cell division has taken place. Following each of the four A–P oriented cell divisions, ERK1/2 is differentially activated in the posterior sister cells, into which the pigment cell lineage segregates. Eph/ephrin signals are critical during the third A–P oriented cell division to spatially restrict ERK1/2 activation to the posterior daughter cell. Targeted inhibition of Eph/ephrin signals results in, at neurula stages, anterior expansion of both ERK1/2 activation and a pigment cell lineage marker and subsequently, at larval stages, supernumerary pigment cells. We discuss the implications of these findings with respect to the evolution of the vertebrate neural crest.

CACN-1/Cactin Plays a Role in Wnt Signaling in C. elegans

Wnt signaling is tightly regulated during animal development and controls cell proliferation and differentiation. In C. elegans, activation of Wnt signaling alters the activity of the TCF/LEF transcription factor, POP-1, through activation of the Wnt/β-catenin or Wnt/β-catenin asymmetry pathways. In this study, we have identified CACN-1 as a potential regulator of POP-1 in C. elegans larval development. CACN-1/Cactin is a well-conserved protein of unknown molecular function previously implicated in the regulation of several developmental signaling pathways. Here we have used activation of POPTOP, a POP-1-responsive reporter construct, as a proxy for Wnt signaling. POPTOP requires POP-1 and SYS-1/β-catenin for activation in L4 uterine cells. RNAi depletion experiments show that CACN-1 is needed to prevent excessive activation of POPTOP and for proper levels and/or localization of POP-1. Surprisingly, high POPTOP expression correlates with increased levels of POP-1 in uterine nuclei, suggesting POPTOP may not mirror endogenous gene expression in all respects. Genetic interaction studies suggest that CACN-1 may act partially through LIT-1/NLK to alter POP-1 localization and POPTOP activation. Additionally, CACN-1 is required for proper proliferation of larval seam cells. Depletion of CACN-1 results in a loss of POP-1 asymmetry and reduction of terminal seam cell number, suggesting an adoption of the anterior, differentiated fate by the posterior daughter cells. These findings suggest CACN-1/Cactin modulates Wnt signaling during larval development.

Effects of Roscovitine on Schedule of Divisional Morphogenesis, Basal Bodies Proliferation and Cell Divisions in Tetrahymena thermophila

During cell cycle of a ciliate Tetrahymena thermophila the divisions of micro- and macronucleus, cortical morphogenesis and cytokinesis are temporarily coordinated. Cortical morphogenesis begins with proliferation of the new ciliary basal bodies (BBs) within meridional cortical rows of ciliary BBs, and with the local proliferation of BBs, which form the new oral apparatus (OA2), positioned subequatorialy and destined for prospective posterior daughter cell (opisthe). Prior to cytokinesis, two prospective daughter cells are of equal size and show metamery of their cortical patterns. We studied effects of 20 μM roscovitine (an inhibitor of several cyclin-dependent kinases) on the cell cycle progression of T. thermophila. We showed that roscovitine delayed cell division, delayed or arrested macronuclear division and induced increase of cell size and the number of BBs in the cortical rows. The increase in the number of BBs in cortical rows induced cell elongation which was proportional to the increase in cell surface area. There was uncoupling between this BBs proliferation which is continued during prolonged cell cycle and delayed cytokinesis, what resulted in topological alteration of the respective positions of the OA2 and of the contractile vacuole pores (CVPs). In roscovitine treated cells, the new OA2 was positioned subequatorialy, but the fission zone was shifted posterior to the equatorial plane of the cell and positioned across and in the extreme cases behind of the new OA2. This resulted in the formation of a large proter and small size opisthe. The roscovitine treatment induced a formation of a plethora of phenotypes of postdividing cells. We found that irrespective of changes in divisional morphogenesis induced by roscovitine treatment, all mature BBs were associated with the cdc14-like phosphatase. Taken together all these data indicate that during cell cycle of T. thermophila the normal morphology of the daughter cells depends on the proper division of micro- and macronucleus and on temporal control of BBs proliferation along the longitudinal rows, during OA2 stomatogenesis and during selection of BBs involved in differentiation of apical BBs (couplets) and cell division.

Cellular Symmetry Breaking during Caenorhabditis elegans Development

The nematode worm Caenorhabditis elegans has produced a wellspring of insights into mechanisms that govern cellular symmetry breaking during animal development. Here we focus on two highly conserved systems that underlie many of the key symmetry-breaking events that occur during embryonic and larval development in the worm. One involves the interplay between Par proteins, Rho GTPases, and the actomyosin cytoskeleton and mediates asymmetric cell divisions that establish the germline. The other uses elements of the Wnt signaling pathway and a highly reiterative mechanism that distinguishes anterior from posterior daughter cell fates. Much of what we know about these systems comes from intensive study of a few key events-Par/Rho/actomyosin-mediated polarization of the zygote in response to a sperm-derived cue and the Wnt-mediated induction of endoderm at the four-cell stage. However, a growing body of work is revealing how C. elegans exploits elements/variants of these systems to accomplish a diversity of symmetry-breaking tasks throughout embryonic and larval development.

Asymmetric Rab11 Endosomes Regulate Delta Recycling and Specify Cell Fate in the Drosophila Nervous System

Drosophila sensory organ precursor (SOP) cells are a well-studied model system for asymmetric cell division. During SOP division, the determinants Numb and Neuralized segregate into the pIIb daughter cell and establish a distinct cell fate by regulating Notch/Delta signaling. Here, we describe a Numb- and Neuralized-independent mechanism that acts redundantly in cell-fate specification. We show that trafficking of the Notch ligand Delta is different in the two daughter cells. In pIIb, Delta passes through the recycling endosome which is marked by Rab 11. In pIIa, however, the recycling endosome does not form because the centrosome fails to recruit Nuclear fallout, a Rab 11 binding partner that is essential for recycling endosome formation. Using a mammalian cell culture system, we demonstrate that recycling endosomes are essential for Delta activity. Our results suggest that cells can regulate signaling pathways and influence their developmental fate by inhibiting the formation of individual endocytic compartments.

MOM-5 Frizzled regulates the distribution of DSH-2 to control C. elegans asymmetric neuroblast divisions

Asymmetric cell divisions produce all 302 neurons of the C. elegans hermaphrodite. Here, we describe a role for a C. elegans Dishevelled homolog, DSH-2, in an asymmetric neuroblast division. In dsh-2 mutants, neurons normally descended from the anterior neuroblast daughter of the ABpl/rpppa blast cell were frequently duplicated, while non-neuronal cells produced by the posterior daughter cell were often missing. These observations indicate that in the absence of dsh-2 function, the posterior daughter cell was transformed into a second anterior-like cell. Loss of mom-5, a C. elegans frizzled homolog, produced a similar phenotype. We also show that the DSH-2 protein localized to the cell cortex in most cells of the embryo. In the absence of MOM-5/Fz, DSH-2 was localized to the cytoplasm, suggesting that MOM-5 regulates asymmetric cell division by controlling the localization of DSH-2. Although all neurons in C. elegans are produced by an invariant pattern of cell divisions, our results indicate that cell signaling may contribute to asymmetric neuroblast division during embryogenesis.

Separate and Unequal

DEVELOPMENT When a cell divides, it often does not produce two equivalent daughter cells. For instance, in the Drosophila sensory bristle lineage, division of the sensory organ precursor cell (pI) generates two cells with different cell fates. Le Borgne and Schweisguth report that the daughter cells differ in Notch signaling: Notch is activated in the anterior daughter cell (pIIa) but is inhibited in the posterior daughter cell (pIIb). This difference in Notch activation is mediated by the unequal distribution of Neuralized, a factor that is required for the endocytosis of the Notch ligand Delta in sensory cells. Neuralized function is conserved from flies to frogs; therefore, the involvement of Neuralized during asymmetric cell division may also be found in other animals, including vertebrates. — BAP Dev. Cell 5 , 139 (2003).

A natural strain of Paramecium bursaria lacking symbiotic algae

Paramecium bursaria contains hundreds of algae in its cytoplasm as symbionts and retains them over many generations. Recently, aposymbiotic cells of P. bursaria were collected from a pond. To know whether the natural aposymbiotic strain (Ysa2) lost ability to associate with algae, infection experiments were performed using symbiotic algae isolated from green paramecia. Results showed that Ysa2 establish symbiotic association in the same way as artificially obtained aposymbiotic cells (control). However, clustered algae appeared in some Ysa2 cells after infection. Algal clusters differ in number and size from cell to cell. Isolation line culture was performed to pursue the fate of cells having algal clusters. Within several cell divisions, some descendants retained large clusters and such cells were sometimes misshapen, ceasing proliferation and eventually dying. At cell division of cluster-bearing cells, unequal distribution of clustered algae occurred because many algal clusters tend to locate in the posterior of the host cell. Most extremely, all algae were distributed to the posterior daughter cell, whereas the anterior daughter cell contained no algae. This is one possible mechanism of production of Ysa2 in nature. From these results, we conclude that Ysa2 can make symbiotic association with potentially symbiotic algae, but they have some incompatibilities with the algae.

The Dynamics of Filamentous Structures in the Apical Band, Oral Crescent, Fission Line and the Postoral Meridional Filament in Tetrahymena thermophila Revealed by Monoclonal Antibody 12G9

The ciliate Tetrahymena thermophila possesses a multitude of cytoskeletal structures whose differentiation is related to the basal bodies - the main mediators of the cortical pattern. This investigation deals with immunolocalization using light and electron microscopy of filaments labeled by the monoclonal antibody 12G9, which in other ciliates identifies filaments involved in transmission of cellular polarities and marks cell meridians with the highest morphogenetic potential. In Tetrahymena interphase cells, mAb 12G9 localizes to the sites of basal bodies and to the striated ciliary rootlets, to the apical band of filaments and to the fine fibrillar oral crescent. We followed the sequence of development of these structures during divisional morphogenesis. The labeling of the maternal oral crescent disappears in pre-metaphase cells and reappears during anaphase, concomitantly with differentiation of the new structure in the posterior daughter cell. In the posterior daughter cell, the new apical band originates as small clusters of filaments located at the base of the anterior basal bodies of the apical basal body couplets during early anaphase. The differentiation of the band is completed in the final stages of cytokinesis and in the young post-dividing cell. The maternal band is reorganized earlier, simultaneously with the oral structure. The mAb 12G9 identifies two transient structures present only in dividing cells. One is a medial structure demarcating the two daughter cells during metaphase and anaphase, and defining the new anterior border of the posterior daughter cell. The other is a post-oral meridional filament marking the stomatogenic meridian in postmetaphase cells. Comparative analysis of immunolocalization of transient filaments labeled with mAb12G9 in Tetrahymena and other ciliates indicates that this antibody identifies a protein bound to filamentous structures, which might play a role in relying polarities of cortical domains and could be a part of a mechanism which governs the positioning of cortical organelles in ciliates.

Analysis of the effects of the cdaK1 mutation of Tetrahymena thermophila on the morphogenesis of the fission line

Summary During divisional morphogenesis of a polarized ciliate cell, a single pattern of distribution of cortical structures along the main body axis is gradually transformed into a metameric chain made up of two sets of cortical structures belonging to the prospective anterior and posterior daughter cells. In an advanced stage of division in wild type Tetrahymena thermophila and in the cdaK1 mutant strain grown at the permissive temperature, a fission line boundary appeared in the form of equatorial gaps in the ciliary rows. An epitope of one of the major components of the membrane skeleton (epiplasm) transiently diminished posterior to this fission line and in the vicinities of the anterior and new posterior oral apparatuses. The changes in the distribution of this epitope depended upon the cell cycle. At a restrictive temperature (37°C), cdaK1 mutant cells displayed abnormal phenotypes in a late stage of cell division in cells delayed in cytokinesis. A localized decrease of immunostaining of epiplasm first appeared on the ventral surface of dividing cell along with fission line gaps at the normal central position, with a lengthening of the ventral cortex between oral apparatuses, but was delayed at some other neighbouring longitudes. Fission line gaps appeared at remaining lateral and dorsal longitudes but on anterior latitudes. During cytokinesis, the ventral cortex bulged and formed a ventral protrusion of the prospective anterior daughter cell. This resulted in an anterior translation of the final position of the fission line. An inhibitor of the serine/threonine kinase activity, 6-DMAP, applied to cdaK1 cells at a permissive temperature, yielded some dividing cells exhibiting cdaK1 phenotypes, with similar patterns of decrease of epiplasmic epitope, localized budding off a part of the cortex, and anterior displacement of the fission line. This suggests, a 6-DMAP and temperature-sensitive cell cycle-dependent coupling of patterned growth and subdivision of cell cortex with spatial distribution of the epiplasmic epitope of Tetrahymena. In cdaK1 cells, the post-telophase migration of micronuclei adjusted to the modified anterior position of the defective fission line. This process was arrested by nocodazole but was only indirectly affected by cytochalasin B.

NLK TAKs onto the Wnt signalling pathway

The Wnt signalling pathway regulates cell-fate decisions in development through a complex of β-catenin and the TCF/LEF family of transcription factors. In most experimental systems, Wnt signalling stabilizes cytosolic β-catenin, which then binds to TCF and acts as a transcriptional co-activator. Thus, the loss of β-catenin and TCF results in similar phenotypes. However, in Caenorhabditis elegans, the loss of WRM-1 (a β-catenin homologue) has the opposite effect to the loss of POP-1 (a TCF-related protein). These papers reveal that a novel mitogen-activated protein (MAP) kinase-like pathway converges with the Wnt signalling pathway to regulate TCF-mediated gene transcription1xMAP kinase and Wnt pathways converge to downregulate an HMG-domain repressor in Caenorhabditis elegans. Meneghini, M.D. et al. Nature. 1999; 399: 793–797Crossref | PubMed | Scopus (218)See all References, 2xWRM-1 activates the LIT-1 protein kinase to transduce anterior/posterior polarity signals in C. elegans. Rocheleau, C.E. et al. Cell. 1999; 97: 717–726Abstract | Full Text | Full Text PDF | PubMed | Scopus (202)See all References, 3xThe TAK1–NLK–MAPK-related pathway antagonises signalling between β-catenin and transcription factor TCF. Ishitani, T. et al. Nature. 1999; 399: 798–802Crossref | PubMed | Scopus (423)See all References. This pathway might be the basis for the apparent discrepancy between the role of β-catenin in C. elegans and vertebrates.In C. elegans, Wnt signalling polarizes the embryo by downregulating POP-1 activity in posterior daughter cells. The proteins MOM-1 and LIT-1 are also required to downregulate POP-11xMAP kinase and Wnt pathways converge to downregulate an HMG-domain repressor in Caenorhabditis elegans. Meneghini, M.D. et al. Nature. 1999; 399: 793–797Crossref | PubMed | Scopus (218)See all References, 2xWRM-1 activates the LIT-1 protein kinase to transduce anterior/posterior polarity signals in C. elegans. Rocheleau, C.E. et al. Cell. 1999; 97: 717–726Abstract | Full Text | Full Text PDF | PubMed | Scopus (202)See all References and are homologous to TAK1 (transforming-growth-factor-β-activated kinase 1) and NLK (nemo-like kinase) respectively, which are components of the MAP kinase pathway. Ishitani and colleagues3xThe TAK1–NLK–MAPK-related pathway antagonises signalling between β-catenin and transcription factor TCF. Ishitani, T. et al. Nature. 1999; 399: 798–802Crossref | PubMed | Scopus (423)See all References3 found that TAK1 and NLK negatively regulate β-catenin/TCF-mediated transcription in mammalian cells. TAK1 stimulates the kinase activity of NLK, and this in turn phosphorylates hTCF4. Phosphorylated hTCF4 can still bind to β-catenin, but NLK phosphorylation interferes with the binding of the β-catenin–TCF complex to DNA, thereby negatively regulating β-catenin–TCF-mediated transcription. NLK immunoprecipitates contain hTCF4, but the interaction does not appear to be direct and might require β-catenin3xThe TAK1–NLK–MAPK-related pathway antagonises signalling between β-catenin and transcription factor TCF. Ishitani, T. et al. Nature. 1999; 399: 798–802Crossref | PubMed | Scopus (423)See all References3. Consistent with this, in C. elegans, WRM-1 (β-catenin) was found in a stable complex with LIT-1 (NLK), where it activated LIT-1-dependent kinase activity to hyperphosphorylate POP-1 (TCF). However, unlike the situation in vertebrates, WRM-1 did not form a stable complex with POP-12xWRM-1 activates the LIT-1 protein kinase to transduce anterior/posterior polarity signals in C. elegans. Rocheleau, C.E. et al. Cell. 1999; 97: 717–726Abstract | Full Text | Full Text PDF | PubMed | Scopus (202)See all References2. Interestingly, POP-1 was normally found in the nucleus of vertebrate cells (as it is in C. elegans embryos), but coexpression of POP-1 with LIT-1 and WRM-1 resulted in a redistribution of POP-1 to the cytoplasm2xWRM-1 activates the LIT-1 protein kinase to transduce anterior/posterior polarity signals in C. elegans. Rocheleau, C.E. et al. Cell. 1999; 97: 717–726Abstract | Full Text | Full Text PDF | PubMed | Scopus (202)See all References2. Thus, in C. elegans, the accumulation of WRM-1 due to Wnt signalling might promote the inactivation of POP-1 through LIT-1 rather than promoting the coactivation of POP-1-mediated transcription.

MAP kinase and Wnt pathways converge to downregulate an HMG-domain repressor in Caenorhabditis elegans.

The signalling protein Wnt regulates transcription factors containing high-mobility-group (HMG) domains to direct decisions on cell fate during animal development. In Caenorhabditis elegans, the HMG-domain-containing repressor POP-1 distinguishes the fates of anterior daughter cells from their posterior sisters throughout development, and Wnt signalling downregulates POP-1 activity in one posterior daughter cell called E. Here we show that the genes mom-4 and lit-1 are also required to downregulate POP-1, not only in E but also in other posterior daughter cells. Consistent with action in a common pathway, mom-4 and lit-1 exhibit similar mutant phenotypes and encode components of the mitogen-activated protein kinase (MAPK) pathway that are homologous to vertebrate transforming-growth-factor-beta-activated kinase (TAK1) and NEMO-like kinase (NLK), respectively. Furthermore, MOM-4 and TAK1 bind related proteins that promote their kinase activities. We conclude that a MAPK-related pathway cooperates with Wnt signal transduction to downregulate POP-1 activity. These functions are likely to be conserved in vertebrates, as TAK1 and NLK can downregulate HMG-domain-containing proteins related to POP-1.

WRM-1 Activates the LIT-1 Protein Kinase to Transduce Anterior/Posterior Polarity Signals in C. elegans

During C. elegans development, Wnt/WG signaling is required for differences in cell fate between sister cells born from anterior/posterior divisions. A β-catenin-related gene, wrm-1, and the lit-1 gene are effectors of this signaling pathway and appear to downregulate the activity of POP-1, a TCF/LEF–related protein, in posterior daughter cells. We show here that lit-1 encodes a serine/threonine protein kinase homolog related to the Drosophila tissue polarity protein Nemo. We demonstrate that the WRM-1 protein binds to LIT-1 in vivo and that WRM-1 can activate the LIT-1 protein kinase when coexpressed in vertebrate tissue culture cells. This activation leads to phosphorylation of POP-1 and to apparent changes in its subcellular localization. Our findings provide evidence for novel regulatory avenues for an evolutionarily conserved Wnt/WG signaling pathway.

Regional Differentiation of Cortical Structures and Their Reorganization during Cell Division in Paramecium trichium

We observed the cell surface of Paramecium trichium using three different methods. A non‐dividing paramecium's cell surface consisted of three major regions outside of the oral apparatus: a) an oral groove region, with 2‐cilia‐2‐basal‐body (2C‐2BB) units; b) a posterior region, occupying 1/4 to 1/5 of the cell surface, with 1‐cilium‐l‐basal‐body (1C‐1BB) units; c) the remainder, with l‐cilium‐2‐basal‐body (1C‐2BB) units. Five kinds of region‐specific cortical reorganization occurred prior to cytokinesis: the 2C‐2BB and 1C‐1BB units were not duplicated, while the 1C‐2BB units were reorganized to 2C‐2BB, 1C‐2BB or 1C‐1BB units. These reorganizations of the cell surface progressed from the fission line to the anterior in the prospective anterior daughter cell, and to the posterior in the prospective posterior daughter cell, and bilaterally from the old and also newly developing oral apparatus in both daughter cells. In contrast, the development of cilia and their associated structures in each of the cortical units always progressed from posterior to anterior. The present work also showed that two fission lines began to develop bilaterally from the oral primordium, and then they joined to become a single fission line at the dorsal surface.