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Article ; Online: Toxicidade do nitrito para o camarão Litopenaeus vannamei cultivado em sistemas de água clara e bioflocos

Fabiana Penalva de MELO / Maria Gabriela Padilha FERREIRA / Ítalo Felipe Mascena BRAGA / Eudes de Souza CORREIA

Boletim do Instituto de Pesca, Vol 42, Iss

2016 Volume 4

Abstract: ... concentrações de N-nitrito (0-Controle, 10, 20 e 40 mg N-NO2 L-1) e dois sistemas de cultivo (água clara ...

Abstract	O objetivo deste trabalho foi avaliar a toxicidade do nitrito sobre o crescimento, sobrevivência e quantidade de hemócitos totais na hemolinfa de juvenis do camarão Litopenaeus vannamei (1,60Â±0,06 g) submetidos a diferentes concentrações de N-nitrito e dois sistemas de cultivo. Os camarões foram distribuídos em 24 unidades experimentais (área de 0,20 m2 e volume útil de 30 L), numa densidade de 75 camarões m-2, em um delineamento experimental inteiramente casualizado, em esquema fatorial 2x2, com quatro concentrações de N-nitrito (0-Controle, 10, 20 e 40 mg N-NO2 L-1) e dois sistemas de cultivo (água clara e bioflocos). Os juvenis de L. vannamei foram alimentados com ração comercial (35% proteína bruta). As concentrações de N-NO2 influenciaram significativamente (P<0,05) o peso final (1,71 a 3,36 g), a sobrevivência (40,7 a 96,3 %) e a taxa de crescimento específico (0,15 a 2,42 % dia-1). A interação entre as concentrações de N-nitrito e os sistemas de cultivo não influenciaram significativamente (Pâ"°¥0,05) a quantidade total de hemócitos. Desta forma, é possível cultivar o camarão L. vannamei em concentrações de até 20 mg N-NO2 L-1 por um período de 30 dias sem comprometer o crescimento e a sobrevivência.
Keywords	toxicidade subcrônica ; hemócito total ; crescimento ; sobrevivência ; hemolinfa ; Aquaculture. Fisheries. Angling ; SH1-691 ; Environmental sciences ; GE1-350 ; Oceanography ; GC1-1581
Language	English
Publishing date	2016-12-01T00:00:00Z
Publisher	Instituto de Pesca
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Metabolic heterogeneity and cross-feeding within isogenic yeast populations captured by DILAC.

Kamrad, Stephan / Correia-Melo, Clara / Szyrwiel, Lukasz / Aulakh, Simran Kaur / Bähler, Jürg / Demichev, Vadim / Mülleder, Michael / Ralser, Markus

Nature microbiology

2023 Volume 8, Issue 3, Page(s) 441–454

Abstract: Genetically identical cells are known to differ in many physiological parameters such as growth rate and drug tolerance. Metabolic specialization is believed to be a cause of such phenotypic heterogeneity, but detection of metabolically divergent ... ...

Abstract	Genetically identical cells are known to differ in many physiological parameters such as growth rate and drug tolerance. Metabolic specialization is believed to be a cause of such phenotypic heterogeneity, but detection of metabolically divergent subpopulations remains technically challenging. We developed a proteomics-based technology, termed differential isotope labelling by amino acids (DILAC), that can detect producer and consumer subpopulations of a particular amino acid within an isogenic cell population by monitoring peptides with multiple occurrences of the amino acid. We reveal that young, morphologically undifferentiated yeast colonies contain subpopulations of lysine producers and consumers that emerge due to nutrient gradients. Deconvoluting their proteomes using DILAC, we find evidence for in situ cross-feeding where rapidly growing cells ferment and provide the more slowly growing, respiring cells with ethanol. Finally, by combining DILAC with fluorescence-activated cell sorting, we show that the metabolic subpopulations diverge phenotypically, as exemplified by a different tolerance to the antifungal drug amphotericin B. Overall, DILAC captures previously unnoticed metabolic heterogeneity and provides experimental evidence for the role of metabolic specialization and cross-feeding interactions as a source of phenotypic heterogeneity in isogenic cell populations.
MeSH term(s)	Saccharomyces cerevisiae/metabolism ; Amino Acids/metabolism ; Isotope Labeling
Chemical Substances	Amino Acids
Language	English
Publishing date	2023-02-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2058-5276
ISSN (online)	2058-5276
DOI	10.1038/s41564-022-01304-8
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Self-Establishing Communities: A Yeast Model to Study the Physiological Impact of Metabolic Cooperation in Eukaryotic Cells.

Campbell, Kate / Correia-Melo, Clara / Ralser, Markus

Methods in molecular biology (Clifton, N.J.)

2019 Volume 2049, Page(s) 263–282

Abstract: All biosynthetically active cells are able to export and import metabolites, the small molecule intermediaries of metabolism. In dense cell populations, this hallmark of cells results in the intercellular exchange of a wide spectrum of metabolites. Such ... ...

Abstract	All biosynthetically active cells are able to export and import metabolites, the small molecule intermediaries of metabolism. In dense cell populations, this hallmark of cells results in the intercellular exchange of a wide spectrum of metabolites. Such metabolite exchange enables metabolic specialization of individual cells, leading to far reaching biological implications, as a consequence of the intrinsic connection between metabolism and cell physiology. In this chapter, we discuss methods on how to study metabolite exchange interactions by using self-establishing metabolically cooperating communities (SeMeCos) in the budding yeast Saccharomyces cerevisiae. SeMeCos exploit the stochastic segregation of episomes to progressively increase the number of essential metabolic interdependencies in a community that grows out from an initially prototrophic cell. By coupling genotype to metabotype, SeMeCos allow for the tracking of cells while they specialize metabolically and hence the opportunity to study their progressive change in physiology.
MeSH term(s)	Eukaryotic Cells/metabolism ; Genotype ; Microbial Interactions ; Saccharomyces cerevisiae/metabolism
Language	English
Publishing date	2019-10-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-9736-7_16
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Pyphe

Kamrad, Stephan / Rodríguez-López, María / Cotobal, Cristina / Correia-Melo, Clara / Ralser, Markus / Bähler, Jürg

eLife

2020 Volume 9

Abstract: Microbial fitness screens are a key technique in functional genomics. We present an all-in-one solution, ...

Abstract	Microbial fitness screens are a key technique in functional genomics. We present an all-in-one solution,
MeSH term(s)	Cell Survival ; Colony Count, Microbial/instrumentation ; Colony Count, Microbial/methods ; Gene Deletion ; Genetic Fitness ; Phenotype ; Schizosaccharomyces/genetics ; Schizosaccharomyces/growth & development ; Schizosaccharomyces/physiology ; Software
Language	English
Publishing date	2020-06-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.55160
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Article ; Online: Powering senescence: The ugly side of mitochondria.

Correia-Melo, Clara / Birch, Jodie / Passos, João F

Cell cycle (Georgetown, Tex.)

2016 Volume 15, Issue 19, Page(s) 2541–2542

MeSH term(s)	Aging ; Cellular Senescence ; Mitochondria
Language	English
Publishing date	2016-07-11
Publishing country	United States
Document type	Editorial
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
DOI	10.1080/15384101.2016.1204852
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Article: Demystifying the role of mitochondria in senescence.

Correia-Melo, Clara / Passos, João F

Molecular & cellular oncology

2016 Volume 3, Issue 4, Page(s) e1162896

Abstract: In a study published in The EMBO Journal, we demonstrated that mitochondria are necessary for the proinflammatory phenotype of senescence. Furthermore, we identified a new senescence-regulatory pathway involving mTOR-dependent mitochondrial biogenesis. ... ...

Abstract	In a study published in The EMBO Journal, we demonstrated that mitochondria are necessary for the proinflammatory phenotype of senescence. Furthermore, we identified a new senescence-regulatory pathway involving mTOR-dependent mitochondrial biogenesis. These data highlight mitochondria as targets for interventions that counteract the pro-aging effects of senescence while preserving tumor suppression.
Language	English
Publishing date	2016-03-28
Publishing country	United States
Document type	Journal Article
ISSN	2372-3556
ISSN	2372-3556
DOI	10.1080/23723556.2016.1162896
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Article ; Online: Inorganic sulfur fixation via a new homocysteine synthase allows yeast cells to cooperatively compensate for methionine auxotrophy.

Yu, Jason S L / Heineike, Benjamin M / Hartl, Johannes / Aulakh, Simran K / Correia-Melo, Clara / Lehmann, Andrea / Lemke, Oliver / Agostini, Federica / Lee, Cory T / Demichev, Vadim / Messner, Christoph B / Mülleder, Michael / Ralser, Markus

PLoS biology

2022 Volume 20, Issue 12, Page(s) e3001912

Abstract: The assimilation, incorporation, and metabolism of sulfur is a fundamental process across all domains of life, yet how cells deal with varying sulfur availability is not well understood. We studied an unresolved conundrum of sulfur fixation in yeast, in ... ...

Abstract	The assimilation, incorporation, and metabolism of sulfur is a fundamental process across all domains of life, yet how cells deal with varying sulfur availability is not well understood. We studied an unresolved conundrum of sulfur fixation in yeast, in which organosulfur auxotrophy caused by deletion of the homocysteine synthase Met17p is overcome when cells are inoculated at high cell density. In combining the use of self-establishing metabolically cooperating (SeMeCo) communities with proteomic, genetic, and biochemical approaches, we discovered an uncharacterized gene product YLL058Wp, herein named Hydrogen Sulfide Utilizing-1 (HSU1). Hsu1p acts as a homocysteine synthase and allows the cells to substitute for Met17p by reassimilating hydrosulfide ions leaked from met17Δ cells into O-acetyl-homoserine and forming homocysteine. Our results show that cells can cooperate to achieve sulfur fixation, indicating that the collective properties of microbial communities facilitate their basic metabolic capacity to overcome sulfur limitation.
MeSH term(s)	Cysteine/metabolism ; Cysteine Synthase/genetics ; Cysteine Synthase/metabolism ; Methionine/metabolism ; Proteomics ; Racemethionine ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae/metabolism ; Sulfur/metabolism
Chemical Substances	Cysteine (K848JZ4886) ; Cysteine Synthase (EC 2.5.1.47) ; MET17 protein, S cerevisiae (EC 2.5.1.47) ; Methionine (AE28F7PNPL) ; O-acetylhomoserine (thiol)-lyase (EC 2.5.1.47) ; Racemethionine (73JWT2K6T3) ; Sulfur (70FD1KFU70) ; YLL058W protein, S cerevisiae (EC 2.5.1.48)
Language	English
Publishing date	2022-12-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2126776-5
ISSN	1545-7885 ; 1544-9173
ISSN (online)	1545-7885
ISSN	1544-9173
DOI	10.1371/journal.pbio.3001912
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Article: Mitochondria: Are they causal players in cellular senescence?

Correia-Melo, Clara / Passos, João F

Biochimica et biophysica acta

2015 Volume 1847, Issue 11, Page(s) 1373–1379

Abstract: Cellular senescence entails an irreversible cell-cycle arrest characterised by drastic cytomorphological and metabolic changes. In recent years, the implications of cellular senescence in physiological and pathological settings, such as ageing and cancer, ...

Abstract	Cellular senescence entails an irreversible cell-cycle arrest characterised by drastic cytomorphological and metabolic changes. In recent years, the implications of cellular senescence in physiological and pathological settings, such as ageing and cancer, have gained firm ground. It is, therefore, important to understand the mechanisms underpinning the establishment and maintenance of senescence. Age-dependent alterations in cellular metabolic processes are greatly driven by changes in mitochondrial function and homeostasis. Classically, mitochondrial dysfunction has been implicated in cellular senescence mainly by promoting oxidative damage-induced cell-cycle arrest; however, emerging data suggests that other mitochondrial-dependent factors play an important role in the induction of senescent phenotypes. Here we review the role of mitochondrial homeostatic mechanisms, mitochondrial metabolites and ROS generation in the signalling pathways leading to the induction and maintenance of cellular senescence and discuss how this may contribute to the ageing process. This article is part of a Special Issue entitled: Mitochondrial Dysfunction in Aging.
MeSH term(s)	Animals ; Cellular Senescence ; Electron Transport ; Homeostasis ; Humans ; Mitochondria/physiology ; Reactive Oxygen Species/metabolism
Chemical Substances	Reactive Oxygen Species
Language	English
Publishing date	2015-05-28
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbabio.2015.05.017
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Article ; Online: Pyphe, a python toolbox for assessing microbial growth and cell viability in high-throughput colony screens

Stephan Kamrad / María Rodríguez-López / Cristina Cotobal / Clara Correia-Melo / Markus Ralser / Jürg Bähler

eLife, Vol

2020 Volume 9

Abstract: Microbial fitness screens are a key technique in functional genomics. We present an all-in-one solution, pyphe, for automating and improving data analysis pipelines associated with large-scale fitness screens, including image acquisition and ... ...

Abstract	Microbial fitness screens are a key technique in functional genomics. We present an all-in-one solution, pyphe, for automating and improving data analysis pipelines associated with large-scale fitness screens, including image acquisition and quantification, data normalisation, and statistical analysis. Pyphe is versatile and processes fitness data from colony sizes, viability scores from phloxine B staining or colony growth curves, all obtained with inexpensive transilluminating flatbed scanners. We apply pyphe to show that the fitness information contained in late endpoint measurements of colony sizes is similar to maximum growth slopes from time series. We phenotype gene-deletion strains of fission yeast in 59,350 individual fitness assays in 70 conditions, revealing that colony size and viability provide complementary, independent information. Viability scores obtained from quantifying the redness of phloxine-stained colonies accurately reflect the fraction of live cells within colonies. Pyphe is user-friendly, open-source and fully documented, illustrated by applications to diverse fitness analysis scenarios.
Keywords	genetic screen ; phenomics ; python software ; microbial fitness ; high-throughput phenotyping ; cell viability ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
Subject code	612
Language	English
Publishing date	2020-06-01T00:00:00Z
Publisher	eLife Sciences Publications Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Mitochondria: Are they causal players in cellular senescence?

Correia-Melo, Clara / João F. Passos

Biochimica et biophysica acta. 2015 Nov., v. 1847, no. 11

2015

Abstract	Cellular senescence entails an irreversible cell-cycle arrest characterised by drastic cytomorphological and metabolic changes. In recent years, the implications of cellular senescence in physiological and pathological settings, such as ageing and cancer, have gained firm ground. It is, therefore, important to understand the mechanisms underpinning the establishment and maintenance of senescence. Age-dependent alterations in cellular metabolic processes are greatly driven by changes in mitochondrial function and homeostasis. Classically, mitochondrial dysfunction has been implicated in cellular senescence mainly by promoting oxidative damage-induced cell-cycle arrest; however, emerging data suggests that other mitochondrial-dependent factors play an important role in the induction of senescent phenotypes. Here we review the role of mitochondrial homeostatic mechanisms, mitochondrial metabolites and ROS generation in the signalling pathways leading to the induction and maintenance of cellular senescence and discuss how this may contribute to the ageing process. This article is part of a Special Issue entitled: Mitochondrial Dysfunction in Aging.
Keywords	cell cycle checkpoints ; cell senescence ; homeostasis ; metabolites ; mitochondria ; neoplasms ; phenotype ; signal transduction
Language	English
Dates of publication	2015-11
Size	p. 1373-1379.
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	282711-6
ISSN	0005-2728 ; 0304-4173
ISSN	0005-2728 ; 0304-4173
DOI	10.1016/j.bbabio.2015.05.017
Database	NAL-Catalogue (AGRICOLA)

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