Anterior 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.

Wnt signaling polarizes cortical actin polymerization to increase daughter cell asymmetry

Asymmetric positioning of the mitotic spindle contributes to the generation of two daughter cells with distinct sizes and fates. Here, we investigated an asymmetric division in the Caenorhabditis elegans Q neuroblast lineage. In this division, beginning with an asymmetrically positioned spindle, the daughter-cell size differences continuously increased during cytokinesis, and the smaller daughter cell in the posterior eventually underwent apoptosis. We found that Arp2/3-dependent F-actin assembled in the anterior but not posterior cortex during division, suggesting that asymmetric expansion forces generated by actin polymerization may enlarge the anterior daughter cell. Consistent with this, inhibition of cortical actin polymerization or artificially equalizing actin assembly led to symmetric cell division. Furthermore, disruption of the Wnt gradient or its downstream components impaired asymmetric cortical actin assembly and caused symmetric division. Our results show that Wnt signaling establishes daughter cell asymmetry by polarizing cortical actin polymerization in a dividing cell.

Caudal-dependent cell positioning directs morphogenesis of the C. elegans ventral epidermis

Strikingly, epithelial morphogenesis remains incomplete at the end of C. elegans embryonic development; newly hatched larvae undergo extensive remodelling of their ventral epidermis during the first larval stage (L1), when newly-born epidermal cells move ventrally to complete the epidermal syncytium. Prior to this remodelling, undivided lateral seam cells produce anterior adherens junction processes that are inherited by the anterior daughter cells following an asymmetric division during L1. These adherens junction processes provide the ventral migratory route for these anterior daughters. Here, we show that these processes are perturbed in pal-1/caudal mutant animals, resulting in their inheritance by posterior, seam-fated daughters. This causes aberrant migration of seam daughter cells, disrupting the ventral epidermis. Using 4D-lineaging, we demonstrate that this larval epidermal morphogenesis defect in pal-1 mutants can be traced directly back to an initial cell positioning defect in the embryo. pal-1 expression, driven by a single intronic enhancer, is required to correctly position the seam cells in embryos such that the appropriate cell junctions support the correct migratory paths of seam daughters later in development, irrespective of their fate. Thus, during ventral epithelial remodelling in C. elegans, we show that the position of migrating cells, specified by pal-1/caudal, appears to be more important than their fate in driving morphogenesis.

The Caenorhabditis elegans gene ham-1 regulates daughter cell size asymmetry primarily in divisions that produce a small anterior daughter cell

C. elegans cell divisions that produce an apoptotic daughter cell exhibit Daughter Cell Size Asymmetry (DCSA), producing a larger surviving daughter cell and a smaller daughter cell fated to die. Genetic screens for mutants with defects in apoptosis identified several genes that are also required for the ability of these divisions to produce daughter cells that differ in size. One of these genes, ham-1, encodes a putative transcription factor that regulates a subset of the asymmetric cell divisions that produce an apoptotic daughter cell. In a survey of C. elegans divisions, we found that ham-1 mutations affect primarily anterior/posterior divisions that produce a small anterior daughter cell. The affected divisions include those that generate an apoptotic cell as well as those that generate two surviving cells. Our findings suggest that HAM-1 primarily promotes DCSA in a certain class of asymmetric divisions.

The Wnt/β-Catenin Asymmetry Pathway Patterns theAtonalOrthologlin-32to Diversify Cell Fate in aCaenorhabditis elegansSensory Lineage

Each sensory ray of the Caenorhabditis elegans male tail comprises three distinct neuroglial cell types. These three cells descend from a single progenitor, the ray precursor cell, through several rounds of asymmetric division called the ray sublineage. Ray development requires the conserved atonal-family bHLH gene lin-32, which specifies the ray neuroblast and promotes the differentiation of its progeny. However, the mechanisms that allocate specific cell fates among these progeny are unknown. Here we show that the distribution of LIN-32 during the ray sublineage is markedly asymmetric, localizing to anterior daughter cells in two successive cell divisions. The anterior-posterior patterning of LIN-32 expression and of differentiated ray neuroglial fates is brought about by the Wnt/β-catenin asymmetry pathway, including the Wnt ligand LIN-44, its receptor LIN-17, and downstream components LIT-1 (NLK), SYS-1 (β-catenin), and POP-1 (TCF). LIN-32 asymmetry itself has an important role in patterning ray cell fates, because the failure to silence lin-32 expression in posterior cells disrupts development of this branch of the ray sublineage. Together, our results illustrate a mechanism whereby the regulated function of a proneural-class gene in a single neural lineage can both specify a neural precursor and actively pattern the fates of its progeny. Moreover, they reveal a central role for the Wnt/β-catenin asymmetry pathway in patterning neural and glial fates in a simple sensory lineage.

Regulation of asymmetric positioning of nuclei by Wnt and Src signaling and its roles in POP‐1/TCF nuclear asymmetry in Caenorhabditis elegans

In various polarized cells, positions of nuclei are often off-center. However, extrinsic signals regulating nuclear off-centering and its biologic roles remain to be elucidated. In Caenorhabditis elegans, polarity of the EMS cell undergoing asymmetric division is regulated by the MOM-2/Wnt and MES-1 signals from its posterior neighbor P2 cell. We show that after divisions of different cells including EMS, the nuclei of the posterior but not anterior daughter cells are anchored to the posterior cell cortex via centrosomes. We also show that this nuclear anchoring is regulated by components of the Wnt pathway and SRC-1 that functions in MES-1 signaling. To understand the biologic roles of nuclear anchoring, we analyzed its effects on asymmetric nuclear localization of POP-1/TCF that is also regulated by Wnt and Src signaling. We found that in mom-2 mutants where the nuclear anchoring and POP-1 asymmetry is partially inhibited, the proximity of the nucleus to the cell cortex correlated with POP-1 asymmetry. Furthermore, in mutants of mom-2, the defect in the anchoring is clearly correlated with that of asymmetric fate determination. These results suggest that the asymmetric nuclear anchoring functions in asymmetric division by enhancing POP-1 asymmetry.

Quantitative Analysis of Protein Dynamics during Asymmetric Cell Division

In dividing Drosophila sensory organ precursor (SOP) cells, the fate determinant Numb and its associated adaptor protein Pon localize asymmetrically and segregate into the anterior daughter cell, where Numb influences cell fate by repressing Notch signaling. Asymmetric localization of both proteins requires the protein kinase aPKC and its substrate Lethal (2) giant larvae (Lgl). Because both Numb and Pon localization require actin and myosin, lateral transport along the cell cortex has been proposed as a possible mechanism for their asymmetric distribution. Here, we use quantitative live analysis of GFP-Pon and Numb-GFP fluorescence and fluorescence recovery after photobleaching (FRAP) to characterize the dynamics of Numb and Pon localization during SOP division. We demonstrate that Numb and Pon rapidly exchange between a cytoplasmic pool and the cell cortex and that preferential recruitment from the cytoplasm is responsible for their asymmetric distribution during mitosis. Expression of a constitutively active form of aPKC impairs membrane recruitment of GFP-Pon. This defect can be rescued by coexpression of nonphosphorylatable Lgl, indicating that Lgl is the main target of aPKC. We propose that a high-affinity binding site is asymmetrically distributed by aPKC and Lgl and is responsible for asymmetric localization of cell-fate determinants during mitosis.

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.

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.

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.

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.

Development of surface pattern during division in Paramecium: III. Study of stomatogenesis in the wild type using antitubulin antibodies and confocal microscopy

Summary Stomatogenesis, during the vegetative division of Paramecium, is a complex morphogenetic process involving massive proliferation of basal bodies and their progressive patterning to generate a new oral apparatus in the immediate vicinity of the old one. This new oral apparatus will be inherited by the posterior daughter cell while the old one remains in the anterior daughter cell. We have carried out a detailed description of the whole process, using new antibodies and confocal microscopy, allowing visualization of all basal bodies and a number of other cytoskeletal elements, thus completing our previous description of morphogenesis. The following inferences could be made: 1) The new oral structures are exclusively formed from the anarchic field by a two step wave of basal body duplication. These two steps strictly parallel, slightly in advance, those we have previously detailed at the level of the “somatic” cortex, suggesting *) that a common set of biochemical cascades is involved, **) that the OA may be triggering these cascades. 2) The initial proliferation of basal bodies occurs in the immediate vicinity of the parental “paroral kinety” which itself remains invariant and appears to dictate the progressive patterning of the oral anlage (as can be inferred from the staining intensity, distance and alignment of the basal bodies of the anarchic field with respect to the paroral kinety). This suggests that the concept of cytotaxis or structural guidance can be extended to the genesis of an elaborate set of basal bodies. 3) The number of basal bodies within the anarchic field is determined during this formation of the new oral apparatus. Thus, the size and possibly part of the pattern of the new OA is determined in one generation, with storage of morphogenetic potentialities used in the next generation. In this process, a slight cortical rotation around the cell axis is effected at each division. 4) The whole morphogenetic assemblage up to the level of the whole cell displays an overall left-right asymmetry which is progressively built up upon the basic asymmetry of the basal body.

Activation of the mec-3 promoter in two classes of stereotyped lineages in Caenorhabditis elegans

The mec-3 gene of Caenorhabditis elegans encodes a homeodomain protein and is expressed in one of two cells upon asymmetric cell division. As a result of asymmetric mec-3 expression, the two sister cells express different fates, so mec-3 is a likely target for the machinery that mediates asymmetric cell division. The unc-86 gene encodes a homeodomain protein of the POU family, which activates mec-3 by binding to its promoter. The ten mec-3-expressing cells are a subset of the anterior daughters of UNC-86-containing cells. Posterior daughters of UNC-86-containing cells do not express mec-3, even though the UNC-86 protein is distributed into both daughter cells. Lineages that express the unc-86 and mec-3 genes can be grouped into two types: in Type I lineages, UNC-86 protein is first made in the immediate parent of the terminal mec-3-expressing cell, while in Type II lineages, UNC-86 is first made in the grandparent of the terminal mec-3-expressing cell. The purpose of experiments presented here is to understand the relationship between the mec-3 expression patterns in each type of lineage, and to determine the fundamental activity pattern of the mec-3 promoter. We find that in the Type I V5.pa lineage, mec-3-lacZ is first synthesized in the terminal PVDR neuron, one cell division after unc-86 is expressed. mec-3 expression in PVDR can occur by transcriptional regulation alone; segregation of the mec-3 RNA or protein is not required to explain the asymmetric expression of mec-3. In the Type II Q lineage, the mec-3 promoter activity can be detected in the immediate anterior daughter of the first unc-86-expressing cell, but when this cell divides, mec-3 is expressed in only one of its daughters at later times. It seems likely that, in the short-lived immediate anterior daughter cell in Type II lineages, mec-3 product does not accumulate to levels that can influence subsequent events. Our results suggest that the mec-3 promoter is activated in all anterior daughters of unc-86-expressing cells.

Asymmetrical cell division in Blepharisma japonicum: Difference between daughter cells in mating-type expression

In cell division of high-frequency-selfers in the ciliate Blepharisma japonicum, daughter cells are different in mating-type expression. The anterior daughter cell is mating type I. The posterior daughter cell is mating type II at first and then changes to mating type I after about 24 h. The anteroposterior polarity of predivision cells appears to correlate with the asymmetrical cell division. This work introduces a unicellular organism about the size of microscopic metazoa as a model system for the study of asymmetrical cell division, which is particularly important in developmental processes.

Stomatogenic Events Accompanying Binary Fission in Blepharisma*

Stomatogenesis was studied in the heterotrich ciliate Blepharisma japonicum stained with protargol. During binary fission not only is a new oral apparatus made for the posterior daughter, but the already existing oral apparatus of the parent cell is reorganized, i.e., partially disassembled and then subsequently reassembled to provide a functional feeding apparatus for the anterior daughter cell. These morphogenetic events, requiring 2 1/2 to 3 hr, are complete by the time the anterior and posterior daughters separate. In preparation for division, an oral anlage is formed by the rapid proliferation of kinetosomes along 4-5 stomatogenic kinetics directly subtending the cytostome. This field of randomly oriented kinetosomes ultimately gives rise to the feeding apparatus of the posterior daughter cell. Early in division, the oral anlage separates into 2 longitudinal fields of kinetosomes: one is destined to give rise to the undulating membrane and the other forms the adoral zone of membranelles. Shorly after the anlage is established posterior to the cytostome, reorganization of the existing functional mouth is initiated. The morphologic changes associated with this dedifferentiation-redifferentiation sequence lead to the formation of an oral apparatus for the anterior daughter and cannot be distinguished from those characteristically seen during physiologic reorganization.

LONGITUDINAL AND TRANSVERSE DIVISION IN TWO CLOSELY RELATED FLAGELLATES

Next article No AccessJournal ArticlesLONGITUDINAL AND TRANSVERSE DIVISION IN TWO CLOSELY RELATED FLAGELLATESL. R. CLEVELANDL. R. CLEVELAND Search for more articles by this author PDFPDF PLUS Add to favoritesDownload CitationTrack CitationsPermissionsReprints Share onFacebookTwitterLinkedInRedditEmail SectionsMoreDetailsFiguresReferencesCited by The Biological Bulletin Volume 74, Number 1February 1938 Published in association with the Marine Biological Laboratory Article DOIhttps://doi.org/10.2307/1537882 Views: 22Total views on this site © 1938 Marine Biological LaboratoryPDF download Crossref reports no articles citing this article.