Centrosome Aurora A gradient ensures single polarity axis in C. elegans embryos

2020 ◽  
Vol 48 (3) ◽  
pp. 1243-1253 ◽  
Author(s):  
Sukriti Kapoor ◽  
Sachin Kotak
Keyword(s):  
Symmetry Breaking ◽  
Cell Fate ◽  
Cell Cortex ◽  
Axis Formation ◽  
Aurora A Kinase ◽  
Aurora A ◽  
C Elegans ◽  
Cell Embryo ◽  
Polarity Establishment

Cellular asymmetries are vital for generating cell fate diversity during development and in stem cells. In the newly fertilized Caenorhabditis elegans embryo, centrosomes are responsible for polarity establishment, i.e. anterior–posterior body axis formation. The signal for polarity originates from the centrosomes and is transmitted to the cell cortex, where it disassembles the actomyosin network. This event leads to symmetry breaking and the establishment of distinct domains of evolutionarily conserved PAR proteins. However, the identity of an essential component that localizes to the centrosomes and promotes symmetry breaking was unknown. Recent work has uncovered that the loss of Aurora A kinase (AIR-1 in C. elegans and hereafter referred to as Aurora A) in the one-cell embryo disrupts stereotypical actomyosin-based cortical flows that occur at the time of polarity establishment. This misregulation of actomyosin flow dynamics results in the occurrence of two polarity axes. Notably, the role of Aurora A in ensuring a single polarity axis is independent of its well-established function in centrosome maturation. The mechanism by which Aurora A directs symmetry breaking is likely through direct regulation of Rho-dependent contractility. In this mini-review, we will discuss the unconventional role of Aurora A kinase in polarity establishment in C. elegans embryos and propose a refined model of centrosome-dependent symmetry breaking.

scholarly journals Centrosome Aurora A gradient ensures a single PAR-2 polarity axis by regulating RhoGEF ECT-2 localization in C. elegans embryos

2018 ◽  
Author(s):  
Sukriti Kapoor ◽  
Sachin Kotak
Keyword(s):  
Spatial Information ◽  
Aurora A Kinase ◽  
Aurora A ◽  
Posterior Cortex ◽  
C Elegans ◽  
Local Inhibition ◽  
Cell Embryo ◽  
Polarity Establishment ◽  
The One ◽  
Cortical Contractility

AbstractThe proper establishment of the cell polarity is essential for development and morphogenesis. In the Caenorhabditis elegans one-cell embryo, a centrosome localized signal provides spatial information that is responsible for generating a single polarity axis. It is hypothesized that such a signal causes local inhibition of cortical actomyosin network in the vicinity of the centrosome. This pivotal event initiates symmetry breaking to direct partitioning of the partition defective proteins (PARs) in the one-cell embryo. However, the molecular nature of the centrosome regulated signal that impinges on the posterior cortex to bring upon cortical anisotropy in the actomyosin network and to promote polarity establishment remains elusive. Here, we discover that Aurora A kinase (AIR-1 in C. elegans) is essential for proper cortical contractility in the one-cell embryo. Loss of AIR-1 causes pronounced cortical contractions on the entire embryo surface during polarity establishment phase, and this creates more than one PAR-2 polarity axis. Moreover, we show that in the absence of AIR-1, centrosome positioning becomes dispensable in dictating the PAR-2 polarity axis. Interestingly, we identify that Rho Guanine Exchange Factor (GEF) ECT-2 acts downstream to AIR-1 to control excess contractility and notably AIR-1 loss affects ECT-2 cortical localization and thereby polarity establishment. Overall, our study unravels a novel insight whereby an evolutionarily conserved kinase Aurora A inhibits promiscuous PAR-2 domain formation and ensures singularity in the polarity establishment axis.

scholarly journals Aurora-A kinase is required for centrosome maturation in Caenorhabditis elegans

2001 ◽  
Vol 155 (7) ◽  
pp. 1109-1116 ◽  
Author(s):  
Eva Hannak ◽  
Matthew Kirkham ◽  
Anthony A. Hyman ◽  
Karen Oegema
Keyword(s):  
Caenorhabditis Elegans ◽  
Fluorescence Intensity ◽  
Maturation Process ◽  
Aurora A Kinase ◽  
Aurora A ◽  
Wild Type ◽  
C Elegans ◽  
Nuclear Envelope Breakdown ◽  
Pericentriolar Material

Centrosomes mature as cells enter mitosis, accumulating γ-tubulin and other pericentriolar material (PCM) components. This occurs concomitant with an increase in the number of centrosomally organized microtubules (MTs). Here, we use RNA-mediated interference (RNAi) to examine the role of the aurora-A kinase, AIR-1, during centrosome maturation in Caenorhabditis elegans. In air-1(RNAi) embryos, centrosomes separate normally, an event that occurs before maturation in C. elegans. After nuclear envelope breakdown, the separated centrosomes collapse together, and spindle assembly fails. In mitotic air-1(RNAi) embryos, centrosomal α-tubulin fluorescence intensity accumulates to only 40% of wild-type levels, suggesting a defect in the maturation process. Consistent with this hypothesis, we find that AIR-1 is required for the increase in centrosomal γ-tubulin and two other PCM components, ZYG-9 and CeGrip, as embryos enter mitosis. Furthermore, the AIR-1–dependent increase in centrosomal γ-tubulin does not require MTs. These results suggest that aurora-A kinases are required to execute a MT-independent pathway for the recruitment of PCM during centrosome maturation.

scholarly journals Aurora A depletion reveals centrosome-independent polarization mechanism in Caenorhabditis elegans

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Kerstin Klinkert ◽  
Nicolas Levernier ◽  
Peter Gross ◽  
Christian Gentili ◽  
Lukas von Tobel ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Symmetry Breaking ◽  
Break Symmetry ◽  
Dependent Manner ◽  
Aurora A Kinase ◽  
Aurora A ◽  
Physical Description ◽  
C Elegans ◽  
Actin Cortex ◽  
Polarization Mechanism

How living systems break symmetry in an organized manner is a fundamental question in biology. In wild-type Caenorhabditis elegans zygotes, symmetry breaking during anterior-posterior axis specification is guided by centrosomes, resulting in anterior-directed cortical flows and a single posterior PAR-2 domain. We uncover that C. elegans zygotes depleted of the Aurora A kinase AIR-1 or lacking centrosomes entirely usually establish two posterior PAR-2 domains, one at each pole. We demonstrate that AIR-1 prevents symmetry breaking early in the cell cycle, whereas centrosomal AIR-1 instructs polarity initiation thereafter. Using triangular microfabricated chambers, we establish that bipolarity of air-1(RNAi) embryos occurs effectively in a cell-shape and curvature-dependent manner. Furthermore, we develop an integrated physical description of symmetry breaking, wherein local PAR-2-dependent weakening of the actin cortex, together with mutual inhibition of anterior and posterior PAR proteins, provides a mechanism for spontaneous symmetry breaking without centrosomes.

scholarly journals Aurora A depletion reveals centrosome-independent polarization mechanism in C.elegans

2018 ◽  
Author(s):  
K. Klinkert ◽  
N. Levernier ◽  
P. Gross ◽  
C. Gentili ◽  
L. von Tobel ◽  
...  
Keyword(s):  
Symmetry Breaking ◽  
Transgenic Animals ◽  
Break Symmetry ◽  
Dependent Manner ◽  
Aurora A Kinase ◽  
Aurora A ◽  
C Elegans ◽  
Actin Cortex ◽  
Self Organized ◽  
Polarization Mechanism

AbstractHow living systems break symmetry in an organized manner is an important question in biology. In C. elegans zygotes, symmetry breaking normally occurs in the vicinity of centrosomes, resulting in anterior-directed cortical flows and establishment of a single posterior PAR-2 domain. Here, we report that zygotes depleted of the Aurora A kinase AIR-1 or of centrosomes establish two posterior domains, one at each pole. Using transgenic animals and microfabricated triangular chambers, we establish that such bipolarity occurs in a PAR-2- and curvature-dependent manner. Furthermore, we develop an integrated physical model of symmetry breaking, establishing that local PAR-dependent weakening of the actin cortex, together with mutual inhibition of anterior and posterior PAR proteins, provides a mechanism for self-organized PAR polarization without functional centrosomes in C. elegans.One Sentence SummaryWe uncover a novel centrosome-independent mechanism of polarization in C. elegans zygotes

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 The role of Aurora-A kinase in the Golgi-dependent control of mitotic entry

2011 ◽  
Vol 1 (2) ◽  
pp. 61-65 ◽  
Author(s):  
Romina Ines Cervigni ◽  
Maria Luisa Barretta ◽  
Angela Persico ◽  
Daniela Corda ◽  
Antonino Colanzi
Keyword(s):  
Aurora A Kinase ◽  
Aurora A ◽  
Mitotic Entry

scholarly journals A cohort of Caenorhabditis species lacking the highly conserved let-7 microRNA

2021 ◽  
Author(s):  
Charles Nelson ◽  
Victor Ambros
Keyword(s):  
Cell Fate ◽  
Nematode Species ◽  
Loss Of Function ◽  
C Elegans ◽  
Adult Transition ◽  
Developmental Progression ◽  
Caenorhabditis Species ◽  
Heterochronic Gene ◽  
Bilaterian Animal

Abstract The let-7 gene encodes a highly conserved microRNA with critical functions integral to cell fate specification and developmental progression in diverse animals. In Caenorhabditis elegans, let-7 is a component of the heterochronic (developmental timing) gene regulatory network, and loss-of-function mutations of let-7 result in lethality during the larval to adult transition due to misregulation of the conserved let-7 target, lin-41. To date, no bilaterian animal lacking let-7 has been characterized. In this study, we identify a cohort of nematode species within the genus Caenorhabditis, closely related to C. elegans, that lack the let-7 microRNA, owing to absence of the let-7 gene. Using C. sulstoni as a representative let-7-lacking species to characterize normal larval development in the absence of let-7, we demonstrate that, except for the lack of let-7, the heterochronic gene network is otherwise functionally conserved. We also report that species lacking let-7 contain a group of divergent let-7 paralogs—also known as the let-7-family of microRNAs—that have apparently assumed the role of targeting the lin-41 mRNA.

scholarly journals Mechanochemical Control of Symmetry Breaking in the Caenorhabditis elegans Zygote

2021 ◽  
Vol 8 ◽  
Author(s):  
Wan Jun Gan ◽  
Fumio Motegi
Keyword(s):  
Caenorhabditis Elegans ◽  
Symmetry Breaking ◽  
Actin Cytoskeleton ◽  
Cell Polarity ◽  
Break Symmetry ◽  
Cell Cortex ◽  
Aurora A Kinase ◽  
Advective Flow ◽  
Polar State ◽  
Cellular Components

Cell polarity is the asymmetric organization of cellular components along defined axes. A key requirement for polarization is the ability of the cell to break symmetry and achieve a spatially biased organization. Despite different triggering cues in various systems, symmetry breaking (SB) usually relies on mechanochemical modulation of the actin cytoskeleton, which allows for advected movement and reorganization of cellular components. Here, the mechanisms underlying SB in Caenorhabditis elegans zygote, one of the most popular models to study cell polarity, are reviewed. A zygote initiates SB through the centrosome, which modulates mechanics of the cell cortex to establish advective flow of cortical proteins including the actin cytoskeleton and partitioning defective (PAR) proteins. The chemical signaling underlying centrosomal control of the Aurora A kinase–mediated cascade to convert the organization of the contractile actomyosin network from an apolar to polar state is also discussed.

scholarly journals PLK-1 Regulation of Asymmetric Cell Division in the Early C. elegans Embryo

2021 ◽  
Vol 8 ◽  
Author(s):  
Amelia J. Kim ◽  
Erik E. Griffin
Keyword(s):  
Cell Division ◽  
Cell Fate ◽  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Asymmetric Cell Division ◽  
Critical Role ◽  
Cell Cortex ◽  
C Elegans ◽  
Mitotic Kinase ◽  
Centrosome Separation

PLK1 is a conserved mitotic kinase that is essential for the entry into and progression through mitosis. In addition to its canonical mitotic functions, recent studies have characterized a critical role for PLK-1 in regulating the polarization and asymmetric division of the one-cell C. elegans embryo. Prior to cell division, PLK-1 regulates both the polarization of the PAR proteins at the cell cortex and the segregation of cell fate determinants in the cytoplasm. Following cell division, PLK-1 is preferentially inherited to one daughter cell where it acts to regulate the timing of centrosome separation and cell division. PLK1 also regulates cell polarity in asymmetrically dividing Drosophila neuroblasts and during mammalian planar cell polarity, suggesting it may act broadly to connect cell polarity and cell cycle mechanisms.

scholarly journals The conserved ASCL1/MASH-1 ortholog HLH-3 specifies sex-specific ventral cord motor neuron fate in C. elegans

2020 ◽  
Author(s):  
Lillian M. Perez ◽  
Aixa Alfonso
Keyword(s):  
Motor Neuron ◽  
Cell Fate ◽  
Motor Neurons ◽  
Bhlh Protein ◽  
Differentiation Markers ◽  
C Elegans ◽  
Ventral Cord ◽  
Neural Specification

ABSTRACTNeural specification can be regulated by one or many transcription factors. Here we identify a novel role for one conserved proneural factor, the bHLH protein HLH-3, implicated in the specification of sex-specific ventral cord motor neurons in C. elegans. In the process of characterizing the role of hlh-3 in neural specification, we document that differentiation of the ventral cord type C neurons, VCs, within their motor neuron class, is dynamic in time and space. Expression of VC class-specific and subclass-specific identity genes is distinct through development and dependent on where they are along the A-P axis (and their position in proximity to the vulva). Our characterization of the expression of VC class and VC subclass-specific differentiation markers in the absence of hlh-3 function reveals that VC fate specification, differentiation, and morphology requires hlh-3 function. Finally, we conclude that hlh-3 cell-autonomously specifies VC cell fate.

Sign in / Sign up

Export Citation Format

Share Document