scholarly journals The nuclear transport factor CSE1 drives macronuclear volume increase and macronuclear node condensation in Stentor coeruleus

2021 ◽  
Author(s):  
Rebecca M McGillivary ◽  
Pranidhi Sood ◽  
Katharine Hammar ◽  
Wallace F Marshall
Keyword(s):  
Cell Division ◽  
Molecular Mechanisms ◽  
Nuclear Transport ◽  
Shape Change ◽  
Developmentally Regulated ◽  
Volume Increase ◽  
Transport Factor ◽  
Single Mass ◽  
Stentor Coeruleus ◽  
The 1960S

The giant ciliate, Stentor coeruleus, provides a unique opportunity to study nuclear shape because its macronucleus undergoes a rapid, dramatic, and developmentally regulated shape change. During a 2 hour time period within cell division and regeneration, the 400 um long moniliform macronucleus condenses into a single mass, elongates into a vermiform shape, and then renodulates, returning to its original beads-on-a-string morphology (Tartar 1961). Previous work from the 1960s - 1980s demonstrated that the macronuclear shape change is a highly regulated part of cell division and regeneration, but there were no molecular studies into this process (De Terra 1964; De Terra 1983). With the recent availability of a sequenced Stentor genome, a transcriptome during regeneration, and molecular tools like RNAi, it is now possible to investigate the molecular mechanisms that drive macronuclear shape change (Slabodnick et al. 2014; Slabodnick et al. 2017; Sood et al. 2021). We found that the volume of the macronucleus increases during condensation. When the nuclear transport factor, CSE1, is knocked down by RNAi, this volume increase is reduced, and the nodes are unable to fuse. This affects the final morphology of the macronucleus: 24 hours after regeneration the macronucleus is misshapen. We found that CSE1 is mainly cytoplasmic during interphase and in early regeneration, and then becomes mainly macronuclear during condensation. At the end of regeneration CSE1 is degraded while the macronucleus returns to its pre-condensation volume. We propose a model in which nuclear transport via CSE1 increases the volume of the macronucleus, driving the condensation of the many nodes into a single mass.

The role of microtubules in chick blastoderm expansion—a quantitative study using colchicine

Development ◽  
1975 ◽  
Vol 34 (1) ◽  
pp. 265-277
Author(s):  
J. R. Downie
Keyword(s):  
Cell Division ◽  
Cell Shape ◽  
Shape Change ◽  
Cell Sheet ◽  
Cell Movement ◽  
Vitelline Membrane ◽  
General Context ◽  
Chick Blastoderm ◽  
Cell Shape Change ◽  
Cytoplasmic Microtubules

Since their discovery, cytoplasmic microtubules have been much studied in the context of cell movement and cell shape change. Much of the work has used drugs, particularly colchicine and its relatives, which break down microtubules — the so-called anti-tubulins. Colchicine inhibits the orientated movements of many cell types in vitro, and disrupts cell shape change in several morphogenetic situations. The investigation reported here used chick blastoderm expansion in New culture in an attempt to quantify the colchicine effect on orientated cell movement. However, although colchicine could halt blastoderm expansion entirely, a simple interpretation was not possible. (1) Colchicine at concentrations capable of blocking mitosis, and of disrupting all or most of the cytoplasmic microtubules of the cells studied, inhibited blastoderm expansion, often resulting in an overall retraction of the cell sheet. (2) Though blastoderm expansion does normally involve considerable cell proliferation, the colchicine effect could not be ascribed to a block on cell division since aminopterin, which stops cell division without affecting microtubules, did not inhibit expansion. (3) Blastoderm expansion is effected by the locomotion of a specialized band of edge cells at the blastoderm periphery. These are the only cells normally attached to the vitelline membrane — the substrate for expansion. When most of the blastoderm was excised, leaving the band of edge cells, and the cultures then treated with colchicine, expansion occurred normally. The colchicine effect on blastoderm expansion could not therefore be ascribed to a direct effect on the edge cells. (4) An alternative site of action of the drug is the remaining cells of the blastoderm. These normally become progressively flatter as expansion proceeds. If flattening in these cells is even partially dependent on their cytoplasmic microtubules, disruption of these microtubules might result in the inherent contractility of the cells resisting and eventually halting edge cell migration. That cell shape in these cells is dependent on microtubules was demonstrated by treating flat blastoderm fragments with colchicine. On incubation, the area occupied by these fragments decreased by 25–30 % more than controls. The significance of these results in the general context of orientated cell movements and cell shape determination is discussed, with particular emphasis on the analogous system of Fundulus epiboly.

scholarly journals The Rho-family GTPase OsRac1 controls rice grain size and yield by regulating cell division

2019 ◽  
Vol 116 (32) ◽  
pp. 16121-16126 ◽  
Author(s):  
Ying Zhang ◽  
Yan Xiong ◽  
Renyi Liu ◽  
Hong-Wei Xue ◽  
Zhenbiao Yang
Keyword(s):  
Grain Size ◽  
Cell Division ◽  
Grain Yield ◽  
Molecular Mechanisms ◽  
Grain Filling ◽  
High Yield ◽  
Rice Grain ◽  
Rop Gtpase ◽  
Key Factor ◽  
Grain Width

Grain size is a key factor for determining grain yield in crops and is a target trait for both domestication and breeding, yet the mechanisms underlying the regulation of grain size are largely unclear. Here we show that the grain size and yield of rice (Oryza sativa) is positively regulated by ROP GTPase (Rho-like GTPase from plants), a versatile molecular switch modulating plant growth, development, and responses to the environment. Overexpression of rice OsRac1ROP not only increases cell numbers, resulting in a larger spikelet hull, but also accelerates grain filling rate, causing greater grain width and weight. As a result, OsRac1 overexpression improves grain yield in O. sativa by nearly 16%. In contrast, down-regulation or deletion of OsRac1 causes the opposite effects. RNA-seq and cell cycle analyses suggest that OsRac1 promotes cell division. Interestingly, OsRac1 interacts with and regulates the phosphorylation level of OsMAPK6, which is known to regulate cell division and grain size in rice. Thus, our findings suggest OsRac1 modulates rice grain size and yield by influencing cell division. This study provides insights into the molecular mechanisms underlying the control of rice grain size and suggests that OsRac1 could serve as a potential target gene for breeding high-yield crops.

scholarly journals Cell growth dilutes the cell cycle inhibitor Rb to trigger cell division

2018 ◽  
Author(s):  
Evgeny Zatulovskiy ◽  
Daniel F. Berenson ◽  
Benjamin R. Topacio ◽  
Jan M. Skotheim
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Cell Growth ◽  
Cell Size ◽  
Mammalian Cells ◽  
Molecular Mechanisms ◽  
Inverse Correlation ◽  
Cell Types ◽  
Similar Amount ◽  
Cell Cycle Inhibitor

Cell size is fundamental to function in different cell types across the human body because it sets the scale of organelle structures, biosynthesis, and surface transport1,2. Tiny erythrocytes squeeze through capillaries to transport oxygen, while the million-fold larger oocyte divides without growth to form the ~100 cell pre-implantation embryo. Despite the vast size range across cell types, cells of a given type are typically uniform in size likely because cells are able to accurately couple cell growth to division3–6. While some genes whose disruption in mammalian cells affects cell size have been identified, the molecular mechanisms through which cell growth drives cell division have remained elusive7–12. Here, we show that cell growth acts to dilute the cell cycle inhibitor Rb to drive cell cycle progression from G1 to S phase in human cells. In contrast, other G1/S regulators remained at nearly constant concentration. Rb is a stable protein that is synthesized during S and G2 phases in an amount that is independent of cell size. Equal partitioning to daughter cells of chromatin bound Rb then ensures that all cells at birth inherit a similar amount of Rb protein. RB overexpression increased cell size in tissue culture and a mouse cancer model, while RB deletion decreased cell size and removed the inverse correlation between cell size at birth and the duration of G1 phase. Thus, Rb-dilution by cell growth in G1 provides a long-sought cell autonomous molecular mechanism for cell size homeostasis.

scholarly journals Balancing dynamic tradeoffs drives cellular reprogramming

2018 ◽  
Author(s):  
Kimberley N. Babos ◽  
Kate E. Galloway ◽  
Kassandra Kisler ◽  
Madison Zitting ◽  
Yichen Li ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cell Division ◽  
Motor Neuron ◽  
Molecular Mechanisms ◽  
Cell Types ◽  
Cellular Reprogramming ◽  
Cellular Event ◽  
Chemical Factors ◽  
Number Of Cells ◽  
Transcription And Replication

AbstractAlthough cellular reprogramming continues to generate new cell types, reprogramming remains a rare cellular event. The molecular mechanisms that limit reprogramming, particularly to somatic lineages, remain unclear. By examining fibroblast-to-motor neuron conversion, we identify a previously unappreciated dynamic between transcription and replication that determines reprogramming competency. Transcription factor overexpression forces most cells into states that are refractory to reprogramming and are characterized by either hypertranscription with little cell division, or hyperproliferation with low transcription. We identify genetic and chemical factors that dramatically increase the number of cells capable of both hypertranscription and hyperproliferation. Hypertranscribing, hyperproliferating cells reprogram at 100-fold higher, near-deterministic rates. We demonstrate that elevated topoisomerase expression endows cells with privileged reprogramming capacity, suggesting that biophysical constraints limit cellular reprogramming to rare events.

scholarly journals Structural genomic applied on the rust fungus Melampsora larici-populina reveals two candidate effector proteins adopting cystine-knot and nuclear transport factor 2-like protein folds

2019 ◽  
Author(s):  
Karine de Guillen ◽  
Cécile Lorrain ◽  
Pascale Tsan ◽  
Philippe Barthe ◽  
Benjamin Petre ◽  
...  
Keyword(s):  
Plant Pathogens ◽  
Nuclear Transport ◽  
Sequence Similarity ◽  
Rust Fungus ◽  
Parasitic Infection ◽  
Effector Proteins ◽  
Host Cells ◽  
Dimensional Structure ◽  
Structural Genomic ◽  
Transport Factor

ABSTRACTRust fungi are plant pathogens that secrete an arsenal of effector proteins interfering with plant functions and promoting parasitic infection. Effectors are often species-specific, evolve rapidly, and display low sequence similarities with known proteins or domains. How rust fungal effectors function in host cells remains elusive, and biochemical and structural approaches have been scarcely used to tackle this question. In this study, we used a strategy based on recombinant protein production in Escherichia coli to study eleven candidate effectors of the leaf rust fungus Melampsora larici-populina. We successfully purified and solved the three-dimensional structure of two proteins, MLP124266 and MLP124017, using NMR spectroscopy. Although both proteins show no sequence similarity with known proteins, they exhibit structural similarities to knottin and nuclear transport factor 2-like proteins, respectively. Altogether, our findings show that sequence-unrelated effectors can adopt folds similar to known proteins, and encourage the use of biochemical and structural approaches to functionally characterize rust effector candidates.

scholarly journals How Many Is Enough? - Challenges of Multinucleated Cell Division in Malaria Parasites

2021 ◽  
Vol 11 ◽  
Author(s):  
Caroline S. Simon ◽  
Vanessa S. Stürmer ◽  
Julien Guizetti
Keyword(s):  
Cell Division ◽  
Molecular Mechanisms ◽  
Multinucleated Cell ◽  
Extrinsic Factors ◽  
Asexual Blood Stage ◽  
Cell Cycles ◽  
Daughter Cells ◽  
Critical Knowledge ◽  
Parasite Multiplication ◽  
Host Parasite

Regulating the number of progeny generated by replicative cell cycles is critical for any organism to best adapt to its environment. Classically, the decision whether to divide further is made after cell division is completed by cytokinesis and can be triggered by intrinsic or extrinsic factors. Contrarily, cell cycles of some species, such as the malaria-causing parasites, go through multinucleated cell stages. Hence, their number of progeny is determined prior to the completion of cell division. This should fundamentally affect how the process is regulated and raises questions about advantages and challenges of multinucleation in eukaryotes. Throughout their life cycle Plasmodium spp. parasites undergo four phases of extensive proliferation, which differ over three orders of magnitude in the amount of daughter cells that are produced by a single progenitor. Even during the asexual blood stage proliferation parasites can produce very variable numbers of progeny within one replicative cycle. Here, we review the few factors that have been shown to affect those numbers. We further provide a comparative quantification of merozoite numbers in several P. knowlesi and P. falciparum parasite strains, and we discuss the general processes that may regulate progeny number in the context of host-parasite interactions. Finally, we provide a perspective of the critical knowledge gaps hindering our understanding of the molecular mechanisms underlying this exciting and atypical mode of parasite multiplication.

scholarly journals Cloning and characterization of hSRP1 , a tissue-specific nuclear transport factor

1998 ◽  
Vol 95 (2) ◽  
pp. 582-587 ◽  
Author(s):  
M. V. Nachury ◽  
U. W. Ryder ◽  
A. I. Lamond ◽  
K. Weis
Keyword(s):  
Nuclear Transport ◽  
Tissue Specific ◽  
Transport Factor

scholarly journals Identification of Hub Genes and Potential Molecular Mechanisms in Patients with HBV-Associated Acute Liver Failure

2020 ◽  
Vol 16 ◽  
pp. 117693432094390
Author(s):  
Ying Sun ◽  
Haitao Yu ◽  
Fangfang Li ◽  
Liqiang Lan ◽  
Daxin He ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Division ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Antigen Processing ◽  
Molecular Mechanisms ◽  
Expression Profiles ◽  
Killer Cell ◽  
Cyclin B1 ◽  
Hub Genes

Hepatitis B virus (HBV) infection is a major cause of acute liver failure (ALF) in China, and mortality rates are high among patients who do not receive a matched liver transplant. This study aimed to determine potential mechanisms involved in HBV-ALF pathogenesis. Gene expression profiles under access numbers GSE38941 and GSE14668 were downloaded from the Gene Expression Omnibus database, including cohorts of HBV-ALF liver tissue and normal samples. Differentially expressed genes (DEGs) with false discovery rates (FDR) <0.05 and |log2(fold change)| >1 as thresholds were screened using the Limma package. Gene modules associated with stable disease were mined using weighed gene co-expression network analysis (WGCNA). A co-expression network was constructed and DEGs were analyzed using gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. A gene-based network was constructed to explore major factors associated with disease progression. We identified 2238 overlapping DEGs as crucial gene cohorts in ALF development. Based on a WGCNA algorithm, 10 modules (modules 1-10) were obtained that ranged from 75 to 1078 genes per module. Cyclin-dependent kinase 1 ( CDK1), cyclin B1 ( CCNB1), and cell-division cycle protein 20 ( CDC20) hub genes were screened using the co-expression network. Furthermore, 17 GO terms and 6 KEGG pathways were identified, such as cell division, immune response process, and antigen processing and presentation. Two overlapping signaling pathways that are crucial factors in HBV-ALF were screened using the Comprehensive Toxicogenomics Database (CTD). Several candidate genes including HLA-E, B2M, HLA-DPA1, and SYK were associated with HBV-ALF progression. Natural killer cell-mediated cytotoxicity and antigen presentation contributed to the progression of HBV-ALF. The HLA-E, B2M, HLA-DPA1, and SYK genes play critical roles in the pathogenesis and development of HBV-ALF.

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