The Regulation of Cell Size

Lloyd, Alison C.

doi:10.1016/j.cell.2013.08.053

Cited by 359 publications

(358 citation statements)

References 86 publications

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“…The cell size dependent metabolism is consistent with allometric scaling of metabolism and provides proliferating cells with the nonlinear functionality critical for cell size homeostasis. 5 Allometric scaling has been suggested to be partly dependent on cell proliferation [33], and cell size control based on metabolism could thus differ between proliferating and non-proliferating cells.…”

Section: Discussionmentioning

confidence: 99%

“…Based on this reasoning, cell size control emerges as a mechanism to ensure appropriate cell physiology and, consequently organismal health, survival and reproduction. 25 However, evidence for this is mostly indirect and correlative: Abnormal cell sizes and increased cell size variability are observed in aging as well as in many common human diseases, including cardiac hypertrophy, type II diabetes, obesity, neurodegenerative diseases and cancer [5]. Coincidentally, these diseases can be classified as metabolic diseases where mitochondrial involvement has been recognized [6].…”

Section: Does Cell Size Matter?mentioning

confidence: 99%

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Mitochondrial Function and Cell Size: An Allometric Relationship

Miettinen

Björklund

2017

Trends in Cell Biology

111

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Allometric scaling of metabolic rate results in lower total mitochondrial oxygen consumption with increasing organismal size. This is considered as a universal law in biology. Here, we discuss how allometric laws impose size dependent limits to mitochondrial activity at the cellular level. This cell size dependent mitochondrial metabolic activity results in nonlinear scaling of metabolism in proliferating cells, which can explain size homeostasis. The allometry in mitochondrial activity can be controlled through mitochondrial fusion and fission machinery, suggesting that mitochondrial connectivity can bypass transport limitations, the presumed biophysical basis for allometry. As physical size affects cellular functionality, cell size dependent metabolism becomes directly relevant for development, metabolic diseases and aging.

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Section: Discussionmentioning

confidence: 99%

Section: Does Cell Size Matter?mentioning

confidence: 99%

Mitochondrial Function and Cell Size: An Allometric Relationship

Miettinen

Björklund

2017

Trends in Cell Biology

111

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“…Large cells, such as neurons and ova, often have specialized mechanisms that allow them to grow to extreme sizes (Lloyd, 2013). It is likely, therefore, that adipocytes have adipocyte-specific pathways that govern their hypertrophic capacity.…”

Section: Specialized Pathways For Regulating Lipid Droplet Size In Admentioning

confidence: 99%

“…A role for mTORC1 in regulating adipocyte size Highly conserved homeostatic mechanisms regulate cell size in eukaryotes (Lloyd, 2013). As adipocyte size is also highly regulated, we reasoned that understanding the core pathways that maintain cell size across multiple diverse cell types has the potential to shed light on the mechanisms controlling adipocyte hypertrophy.…”

Section: Cellular Mechanisms Hypothesized To Regulate Adipose Morphologymentioning

confidence: 99%

Adipose morphology and metabolic disease

Tandon

Wafer

Minchin

2018

Journal of Experimental Biology

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Adipose morphology is defined as the number and size distribution of adipocytes (fat cells) within adipose tissue. Adipose tissue with fewer but larger adipocytes is said to have a 'hypertrophic' morphology, whereas adipose with many adipocytes of a smaller size is said to have a 'hyperplastic' morphology. Hypertrophic adipose morphology is positively associated with insulin resistance, diabetes and cardiovascular disease. By contrast, hyperplastic morphology is associated with improved metabolic parameters. These phenotypic associations suggest that adipose morphology influences risk of cardiometabolic disease. Intriguingly, monozygotic twin studies have determined that adipose morphology is in part determined genetically. Therefore, identifying the genetic regulation of adipose morphology may help us to predict, prevent and ameliorate insulin resistance and associated metabolic diseases. Here, we review the current literature regarding adipose morphology in relation to: (1) metabolic and medical implications; (2) the methods used to assess adipose morphology; and (3) transcriptional differences between morphologies. We further highlight three mechanisms that have been hypothesized to promote adipocyte hypertrophy and thus to regulate adipose morphology.

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“…Given that cell size influences key aspects of cellular function, such as exchanges with the external environment, this rule applies from single-cell organisms to cells within complex tissues in multicellular organisms (Conlon and Raff, 2003;Lloyd, 2013;Mitchison, 2003).…”

Section: Introductionmentioning

confidence: 99%

Molecular control of the Wee1 regulatory pathway by the SAD kinase Cdr2

Guzmán-Vendrell

Rincón

Dingli

et al. 2015

Journal of Cell Science

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Cell growth and division are tightly coordinated to maintain cell size constant during successive cell cycles. In Schizosaccharomyces pombe, the SAD kinase Cdr2 regulates the cell size at division and the positioning of the division plane. Cdr2 forms nodes on the medial cortex containing factors that constitute an inhibitory pathway for Wee1. This pathway is regulated by polar gradients of the DYRK kinase Pom1, and involves a direct inhibitor of Wee1, the SAD kinase Cdr1. Cdr2 also interacts with the anillin Mid1, which defines the division plane, and with additional components of the medial cortical nodes, including Blt1, which participate in the mitotic-promoting and cytokinetic functions of nodes. Here, we show that the interaction of Cdr2 with Wee1 and Mid1 requires the UBA domain of Cdr2, which is necessary for its kinase activity. In contrast, Cdr1 associates with the C-terminus of Cdr2, which is composed of basic and KA-1 lipid-binding domains. Mid1 also interacts with the C-terminus of Cdr2 and might bridge the N-and C-terminal domains, whereas Blt1 associates with the central spacer region. We propose that the association of Cdr2 effectors with different domains might constrain Cdr1 and Wee1 spatially to promote Wee1 inhibition upon Cdr2 kinase activation.

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The Regulation of Cell Size

Cited by 359 publications

References 86 publications

Mitochondrial Function and Cell Size: An Allometric Relationship

Mitochondrial Function and Cell Size: An Allometric Relationship

Adipose morphology and metabolic disease

Molecular control of the Wee1 regulatory pathway by the SAD kinase Cdr2

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