Recent advances in understanding cotton fibre and seed development

The unique feature of the seed of tetraploid cotton (Gossypium hirsutum and Gossypium barbadense) is that about 30% of the seed coat epidermal cells develop into cellulose-enriched fibres, while the embryos synthesize oils and proteins. Hence, both the maternal and filial tissues of the cotton seed are of significant economic value. After initiation from the ovule epidermis at or just before anthesis, the single-celled fibres elongate to 2.5–6.0 cm long in the tetraploid species before they switch to intensive secondary cell wall cellulose synthesis. Thus, apart from its agronomic importance, the cotton fibre represents a model single-cell system to study the control of cell differentiation and elongation, carbon partitioning to cellulose synthesis and also the interaction between maternal (fibre) and embryonic tissues in seeds. Over the past decade or so, significant effort has been made to understand the cellular and molecular basis of cotton fibre development and oil biosynthesis in the embryo. Metabolic engineering of the oil biosynthetic pathway in cotton seed has successfully produced healthier and stable oils. A number of candidate genes and cellular processes that potentially regulate various aspects of fibre development have been identified. Further elucidation of the in vivo functions of those candidate genes could significantly deepen our understanding of fibre development and offer potential for improvement of fibre quality through genetic engineering or marker-assisted breeding approaches.

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Role of gibberellic acid in cotton fibre development

The Journal of Agricultural Science ◽

10.1017/s0021859602001934 ◽

2002 ◽

Vol 138 (3) ◽

pp. 255-260 ◽

Cited By ~ 17

Author(s):

S. J. GOKANI ◽

V. S. THAKER

Keyword(s):

Gibberellic Acid ◽

Fibre Length ◽

Dry Weight ◽

Cotton Fibre ◽

Growth Phases ◽

Fibre Development ◽

The Media

Fibres of three cotton cultivars (Gossypium hirsutum H-4, H-8 and G. arboreum G. Cot-15) were analysed for growth in terms of fibre length and dry weight and endogenous gibberellic acid (GA3) content thrice during 1997–2000, at Rajkot. The development of cotton fibre was divided into four distinct growth phases but overlap between elongation and secondary thickening was considerable which suggests that both these phases are independent of each other. During fibre elongation, GA3 content remained low and increased after a decrease in the rate of fibre elongation in all three genotypes. The long staple cultivar (H-4) showed highest endogenous GA3 content followed by the middle one (H-8) and the short staple cultivar (G. Cot-15). In in vitro studies when GA3, NAA or GA3+NAA was supplemented to the media, increase in fibre length of the short staple cultivar was maximum, followed by the middle one and the long staple cultivar. Both in vivo and in vitro findings suggest that GA3 is one of the important factors that determine fibre length.

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Differential regulation of CaV1.2 channels by cAMP-dependent protein kinase bound to A-kinase anchoring proteins 15 and 79/150

The Journal of General Physiology ◽

10.1085/jgp.201311075 ◽

2014 ◽

Vol 143 (3) ◽

pp. 315-324 ◽

Cited By ~ 24

Author(s):

Matthew D. Fuller ◽

Ying Fu ◽

Todd Scheuer ◽

William A. Catterall

Keyword(s):

Leucine Zipper ◽

Cell System ◽

Differential Regulation ◽

Proteolytic Processing ◽

Channel Activity ◽

Cellular Processes ◽

Anchoring Protein ◽

Cav1.2 Channels ◽

Regulatory Effects

The CaV1.1 and CaV1.2 voltage-gated calcium channels initiate excitation-contraction coupling in skeletal and cardiac myocytes, excitation-transcription coupling in neurons, and many other cellular processes. Up-regulation of their activity by the β-adrenergic–PKA signaling pathway increases these physiological responses. PKA up-regulation of CaV1.2 activity can be reconstituted in a transfected cell system expressing CaV1.2Δ1800 truncated at the in vivo proteolytic processing site, the distal C-terminal domain (DCT; CaV1.2[1801–2122]), the auxiliary α2δ and β subunits of CaV1.2 channels, and A-kinase anchoring protein-15 (AKAP15), which binds to a site in the DCT. AKAP79/150 binds to the same site in the DCT as AKAP15. Here we report that AKAP79 is ineffective in supporting up-regulation of CaV1.2 channel activity by PKA, even though it binds to the same site in the DCT and inhibits the up-regulation of CaV1.2 channel activity supported by AKAP15. Mutation of the calcineurin-binding site in AKAP79 (AKAP79ΔPIX) allows it to support PKA-dependent up-regulation of CaV1.2 channel activity, suggesting that calcineurin bound to AKAP79 rapidly dephosphorylates CaV1.2 channels, thereby preventing their regulation by PKA. Both AKAP15 and AKAP79ΔPIX exert their regulatory effects on CaV1.2 channels in transfected cells by interaction with the modified leucine zipper motif in the DCT. Our results introduce an unexpected mode of differential regulation by AKAPs, in which binding of different AKAPs at a single site can competitively confer differential regulatory effects on the target protein by their association with different signaling proteins.

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A Genetic Screen for Genes That Impact Peroxisomes in Drosophila Identifies Candidate Genes for Human Disease

G3 Genes|Genome|Genetics ◽

10.1534/g3.119.400803 ◽

2019 ◽

Vol 10 (1) ◽

pp. 69-77 ◽

Cited By ~ 2

Author(s):

Hillary K. Graves ◽

Sharayu Jangam ◽

Kai Li Tan ◽

Antonella Pignata ◽

Elaine S. Seto ◽

...

Keyword(s):

Candidate Genes ◽

Selective Constraint ◽

Genetic Screen ◽

Proper Function ◽

Human Populations ◽

Cellular Processes ◽

Oxidative Reactions ◽

Dominant Disease ◽

Size And Morphology

Peroxisomes are subcellular organelles that are essential for proper function of eukaryotic cells. In addition to being the sites of a variety of oxidative reactions, they are crucial regulators of lipid metabolism. Peroxisome loss or dysfunction leads to multi-system diseases in humans that strongly affect the nervous system. In order to identify previously unidentified genes and mechanisms that impact peroxisomes, we conducted a genetic screen on a collection of lethal mutations on the X chromosome in Drosophila. Using the number, size and morphology of GFP tagged peroxisomes as a readout, we screened for mutations that altered peroxisomes based on clonal analysis and confocal microscopy. From this screen, we identified eighteen genes that cause increases in peroxisome number or altered morphology when mutated. We examined the human homologs of these genes and found that they are involved in a diverse array of cellular processes. Interestingly, the human homologs from the X-chromosome collection are under selective constraint in human populations and are good candidate genes particularly for dominant genetic disease. This in vivo screening approach for peroxisome defects allows identification of novel genes that impact peroxisomes in vivo in a multicellular organism and is a valuable platform to discover genes potentially involved in dominant disease that could affect peroxisomes.

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Cortical tension overrides geometrical cues to orient microtubules in confined protoplasts

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.2008895117 ◽

2020 ◽

Vol 117 (51) ◽

pp. 32731-32738

Author(s):

Leia Colin ◽

Antoine Chevallier ◽

Satoru Tsugawa ◽

Florian Gacon ◽

Christophe Godin ◽

...

Keyword(s):

Plant Cells ◽

Cell System ◽

Cellulose Synthesis ◽

Cortical Microtubules ◽

In Planta ◽

Curvature Ratio ◽

Cortical Tension ◽

Maximal Tension

In plant cells, cortical microtubules (CMTs) generally control morphogenesis by guiding cellulose synthesis. CMT alignment has been proposed to depend on geometrical cues, with microtubules aligning with the cell long axis in silico and in vitro. Yet, CMTs are usually transverse in vivo, i.e., along predicted maximal tension, which is transverse for cylindrical pressurized vessels. Here, we adapted a microwell setup to test these predictions in a single-cell system. We confined protoplasts laterally to impose a curvature ratio and modulated pressurization through osmotic changes. We find that CMTs can be longitudinal or transverse in wallless protoplasts and that the switch in CMT orientation depends on pressurization. In particular, longitudinal CMTs become transverse when cortical tension increases. This explains the dual behavior of CMTs in planta: CMTs become longitudinal when stress levels become low, while stable transverse CMT alignments in tissues result from their autonomous response to tensile stress fluctuations.

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A genetic screen for genes that impact peroxisomes in Drosophila identifies candidate genes for human disease

10.1101/704122 ◽

2019 ◽

Author(s):

Hillary K. Graves ◽

Sharayu Jangam ◽

Kai Li Tan ◽

Antonella Pignata ◽

Elaine S. Seto ◽

...

Keyword(s):

Candidate Genes ◽

Selective Constraint ◽

Genetic Screen ◽

Proper Function ◽

Human Populations ◽

Cellular Processes ◽

Oxidative Reactions ◽

Dominant Disease ◽

Size And Morphology

AbstractPeroxisomes are sub-cellular organelles that are essential for proper function of eukaryotic cells. In addition to being the sites of a variety of oxidative reactions, they are crucial regulators of lipid metabolism. Peroxisome loss or dysfunction leads to multisystem diseases in humans that strongly affects the nervous system. In order to uncover previously unidentified genes and mechanisms that impact peroxisomes, we conducted a genetic screen on a collection of lethal mutations on the X chromosome in Drosophila. Using the number, size and morphology of GFP tagged peroxisomes as a readout, we screened for mutations that altered the number and morphology of peroxisomes based on clonal analysis and confocal microscopy. From this screen, we identified 18 genes that cause increases in peroxisome number or altered morphology when mutated. We examined the human homologs of these genes and found that they are involved in a diverse array of cellular processes. Interestingly, the human homologs from the X-chromosome collection are under selective constraint in human populations and are good candidate genes particularly for dominant genetic disease. This in vivo screening approach for peroxisome defects allows identification of novel genes that impact peroxisomes in vivo in a multicellular organism and is a valuable platform to discover genes potentially involved in dominant disease that could affect peroxisomes.

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miR-125b enhances metastasis and progression of cancer via the TXNIP and HIF1α pathway in pancreatic cancer

Cancer Biomarkers ◽

10.3233/cbm-203112 ◽

2021 ◽

pp. 1-12

Author(s):

Pengli Wang ◽

Dan Zheng ◽

Hongyang Qi ◽

Qi Gao

Keyword(s):

Pancreatic Cancer ◽

Hypoxia Inducible Factor ◽

Immunofluorescence Assay ◽

Luciferase Assay ◽

Interacting Protein ◽

Over Expression ◽

Thioredoxin Interacting Protein ◽

Cellular Processes ◽

And Migration

BACKGROUND: MicroRNAs (miRNAs) play potential role in the development of various types of cancer conditions including pancreatic cancer (PC) targeting several cellular processes. Present study was aimed to evaluate function of miR-125b and the mechanism involved in PC. METHODS: Cell migration, MTT and BrdU study was done to establish the migration capability, cell viability and cell proliferation respectively. Binding sites for miR-125b were recognized by luciferase assay, expression of protein by western blot and immunofluorescence assay. In vivo study was done by BALB/c nude xenograft mice for evaluating the function of miR-125b. RESULTS: The study showed that expression of miR-125b was elevated in PC cells and tissues, and was correlated to proliferation and migration of cells. Also, over-expression of miR-125b encouraged migration, metastasis and proliferation of BxPC-3 cells, the suppression reversed it. We also noticed that thioredoxin-interacting protein (TXNIP) was the potential target of miR-125b. The outcomes also suggested that miR-125b governed the expression of TXNIP inversely via directly attaching to the 3′-UTR activating hypoxia-inducible factor 1α (HIF1α). Looking into the relation between HIF1α and TXNIP, we discovered that TXNIP caused the degradation and export of HIF1α by making a complex with it. CONCLUSION: The miR-125b-TXNIP-HIF1α pathway may serve useful strategy for diagnosing and treating PC.

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Fibrosis after Myocardial Infarction: An Overview on Cellular Processes, Molecular Pathways, Clinical Evaluation and Prognostic Value

Medical Sciences ◽

10.3390/medsci9010016 ◽

2021 ◽

Vol 9 (1) ◽

pp. 16

Author(s):

Renato Francesco Maria Scalise ◽

Rosalba De Sarro ◽

Alessandro Caracciolo ◽

Rita Lauro ◽

Francesco Squadrito ◽

...

Keyword(s):

Myocardial Infarction ◽

Signaling Pathways ◽

Ventricular Dysfunction ◽

Healing Process ◽

Molecular Signaling ◽

Cellular Processes ◽

Molecular Signaling Pathways ◽

Fibrotic Scar ◽

Life Threatening

The ischemic injury caused by myocardial infarction activates a complex healing process wherein a powerful inflammatory response and a reparative phase follow and balance each other. An intricate network of mediators finely orchestrate a large variety of cellular subtypes throughout molecular signaling pathways that determine the intensity and duration of each phase. At the end of this process, the necrotic tissue is replaced with a fibrotic scar whose quality strictly depends on the delicate balance resulting from the interaction between multiple actors involved in fibrogenesis. An inflammatory or reparative dysregulation, both in term of excess and deficiency, may cause ventricular dysfunction and life-threatening arrhythmias that heavily affect clinical outcome. This review discusses cellular process and molecular signaling pathways that determine fibrosis and the imaging technique that can characterize the clinical impact of this process in-vivo.

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Zebrafish Models of Autosomal Recessive Ataxias

Cells ◽

10.3390/cells10040836 ◽

2021 ◽

Vol 10 (4) ◽

pp. 836

Author(s):

Ana Quelle-Regaldie ◽

Daniel Sobrido-Cameán ◽

Antón Barreiro-Iglesias ◽

María Jesús Sobrido ◽

Laura Sánchez

Keyword(s):

Animal Models ◽

Autosomal Recessive ◽

Molecular Mechanisms ◽

System Development ◽

Rapid Development ◽

Nervous System Development ◽

Central Nervous System Development ◽

Cellular Processes ◽

Recessive Disorders

Autosomal recessive ataxias are much less well studied than autosomal dominant ataxias and there are no clearly defined systems to classify them. Autosomal recessive ataxias, which are characterized by neuronal and multisystemic features, have significant overlapping symptoms with other complex multisystemic recessive disorders. The generation of animal models of neurodegenerative disorders increases our knowledge of their cellular and molecular mechanisms and helps in the search for new therapies. Among animal models, the zebrafish, which shares 70% of its genome with humans, offer the advantages of being small in size and demonstrating rapid development, making them optimal for high throughput drug and genetic screening. Furthermore, embryo and larval transparency allows to visualize cellular processes and central nervous system development in vivo. In this review, we discuss the contributions of zebrafish models to the study of autosomal recessive ataxias characteristic phenotypes, behavior, and gene function, in addition to commenting on possible treatments found in these models. Most of the zebrafish models generated to date recapitulate the main features of recessive ataxias.

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