What Is The Best Explanation For Increase In Size (Growth) In Any Organism?

Increase in the total cell mass

Cell sectionalisation, growth & proliferation

Prison cell growth refers to an increase in the full mass of a cell, including both cytoplasmic, nuclear and organelle volume.^[1] Cell growth occurs when the overall rate of cellular biosynthesis (production of biomolecules or anabolism) is greater than the overall charge per unit of cellular degradation (the destruction of biomolecules via the proteasome, lysosome or autophagy, or catabolism).^{[two] [3] [4]}

Cell growth is not to be confused with prison cell partition or the cell cycle, which are distinct processes that can occur alongside cell growth during the procedure of cell proliferation, where a cell, known as the "mother jail cell", grows and divides to produce two "daughter cells".^[1] Importantly, cell growth and prison cell division can besides occur independently of i another. During early embryonic development (cleavage of the zygote to grade a morula and blastoderm), cell divisions occur repeatedly without jail cell growth. Conversely, some cells tin can grow without jail cell division or without whatsoever progression of the prison cell cycle, such as growth of neurons during axonal pathfinding in nervous system development.

Cell division without cell growth during embryonic cleavage

In multicellular organisms, tissue growth rarely occurs solely through jail cell growth without cell division, but most oftentimes occurs through cell proliferation.^[1] This is because a unmarried jail cell with only ane copy of the genome in the prison cell nucleus can perform biosynthesis and thus undergo jail cell growth at only one-half the rate of 2 cells. Hence, 2 cells grow (accumulate mass) at twice the rate of a single cell, and four cells grow at four-times the charge per unit of a single cell. This principle leads to an exponential increment of tissue growth charge per unit (mass aggregating) during cell proliferation, attributable to the exponential increase in prison cell number.

Jail cell size depends on both cell growth and cell division, with a disproportionate increase in the rate of cell growth leading to production of larger cells and a disproportionate increment in the charge per unit of cell division leading to production of many smaller cells. Cell proliferation typically involves balanced prison cell growth and cell sectionalization rates that maintain a roughly constant cell size in the exponentially proliferating population of cells.

Some special cells tin grow to very large sizes via an unusual "endoreplication" cell cycle in which the genome is replicated during S-phase simply there is no subsequent mitosis (Chiliad-phase) or prison cell division (cytokinesis). These big endoreplicating cells have many copies of the genome, and then are highly polyploid.

Oocytes can exist unusually large cells in species for which embryonic development takes identify away from the mother's body within an egg that is laid externally. The large size of some eggs can be accomplished either by pumping in cytosolic components from side by side cells through cytoplasmic bridges named ring canals (Drosophila) or by internalisation of nutrient storage granules (yolk granules) by endocytosis (frogs).

Mechanisms of jail cell growth control [edit]

Cells can grow past increasing the overall rate of cellular biosynthesis such that production of biomolecules exceeds the overall rate of cellular degradation of biomolecules via the proteasome, lysosome or autophagy.

Biosynthesis of biomolecules is initiated by expression of genes which encode RNAs and/or proteins, including enzymes that catalyse synthesis of lipids and carbohydrates.

Private genes are generally expressed via transcription into messenger RNA (mRNA) and translation into proteins, and the expression of each factor occurs to various unlike levels in a jail cell-type specific style (in response to gene regulatory networks).

To drive prison cell growth, the global rate of gene expression can be increased by enhancing the overall charge per unit of transcription by RNA polymerase II (for agile genes) or the overall rate of mRNA translation into protein by increasing the abundance of ribosomes and tRNA, whose biogenesis depends on RNA polymerase I and RNA polymerase III. The Myc transcription gene is an example of a regulatory poly peptide that can induce the overall activity of RNA polymerase I, RNA polymerase II and RNA polymerase 3 to drive global transcription and translation and thereby cell growth.

In improver, the activity of individual ribosomes can be increased to boost the global efficiency of mRNA translation via regulation of translation initiation factors, including the 'translational elongation initiation cistron 4E' (eIF4E) circuitous, which binds to and caps the 5' end of mRNAs. The protein TOR, part of the TORC1 complex, is an important upstream regulator of translation initiation too every bit ribosome biogenesis.^[v] TOR is a serine/threonine kinase that can straight phosphorylate and inactivate a general inhibitor of eIF4E, named 4E-bounden protein (4E-BP), to promote translation efficiency. TOR also directly phosphorylates and activates the ribosomal poly peptide S6-kinase (S6K), which promotes ribosome biogenesis.

To inhibit cell growth, the global rate of cistron expression can be decreased or the global rate of biomolecular degradation tin be increased by increasing the rate of autophagy. TOR normally straight inhibits the function of the autophagy inducing kinase Atg1/ULK1. Thus, reducing TOR activeness both reduces the global rate of translation and increases the extent of autophagy to reduce cell growth.

Cell growth regulation in animals [edit]

Many of the signal molecules that control of cellular growth are called growth factors, many of which induce signal transduction via the PI3K/AKT/mTOR pathway, which includes upstream lipid kinase PI3K and the downstream serine/threonine protein kinase Akt, which is able to activate another protein kinase TOR, which promotes translation and inhibits autophagy to drive cell growth.

Nutrient availability influences production of growth factors of the Insulin/IGF-1 family, which broadcast equally hormones in animals to actuate the PI3K/AKT/mTOR pathway in cells to promote TOR activity then that when animals are well fed they will abound rapidly and when they are non able to receive sufficient nutrients they will reduce their growth rate.

In addition, the availability of amino acids to individual cells also directly promotes TOR activity, although this style of regulation is more than important in unmarried-celled organisms than in multicellular organisms such every bit animals that e'er maintain an affluence of amino acids in circulation.

One disputed theory proposes that many unlike mammalian cells undergo size-dependent transitions during the prison cell cycle. These transitions are controlled by the cyclin-dependent kinase Cdk1.^[half-dozen] Though the proteins that control Cdk1 are well understood, their connexion to mechanisms monitoring cell size remains elusive.

A postulated model for mammalian size control situates mass as the driving force of the prison cell cycle. A cell is unable to abound to an abnormally big size because at a certain cell size or jail cell mass, the S stage is initiated. The S stage starts the sequence of events leading to mitosis and cytokinesis. A jail cell is unable to get too small because the after cell cycle events, such every bit S, G2, and Chiliad, are delayed until mass increases sufficiently to begin S phase.^[7]

Cell populations [edit]

Cell populations go through a detail blazon of exponential growth called doubling or prison cell proliferation. Thus, each generation of cells should be twice equally numerous as the previous generation. However, the number of generations only gives a maximum figure as non all cells survive in each generation. Cells tin reproduce in the stage of Mitosis, where they double and split into two genetically equal cells.

Jail cell size [edit]

Jail cell size is highly variable among organisms, with some algae such as Caulerpa taxifolia being a unmarried prison cell several meters in length.^[8] Plant cells are much larger than animal cells, and protists such as Paramecium tin can be 330 μm long, while a typical homo prison cell might be ten μm. How these cells "decide" how big they should be earlier dividing is an open question. Chemical gradients are known to exist partly responsible, and it is hypothesized that mechanical stress detection past cytoskeletal structures is involved. Work on the topic more often than not requires an organism whose prison cell cycle is well-characterized.

Yeast cell size regulation [edit]

The relationship between jail cell size and cell division has been extensively studied in yeast. For some cells, at that place is a mechanism past which cell segmentation is non initiated until a cell has reached a certain size. If the nutrient supply is restricted (after time t = ii in the diagram, beneath), and the rate of increase in cell size is slowed, the fourth dimension menses between cell divisions is increased.^[9] Yeast cell-size mutants were isolated that begin cell sectionalization before reaching a normal/regular size (wee mutants).^[10]

Figure 1:Cell cycle and growth

Wee1 protein is a tyrosine kinase that ordinarily phosphorylates the Cdc2 cell cycle regulatory poly peptide (the homolog of CDK1 in humans), a cyclin-dependent kinase, on a tyrosine residue. Cdc2 drives entry into mitosis by phosphorylating a wide range of targets. This covalent modification of the molecular construction of Cdc2 inhibits the enzymatic activity of Cdc2 and prevents cell division. Wee1 acts to go on Cdc2 inactive during early G2 when cells are still minor. When cells have reached sufficient size during G2, the phosphatase Cdc25 removes the inhibitory phosphorylation, and thus activates Cdc2 to allow mitotic entry. A rest of Wee1 and Cdc25 activity with changes in prison cell size is coordinated past the mitotic entry control system. It has been shown in Wee1 mutants, cells with weakened Wee1 activeness, that Cdc2 becomes agile when the cell is smaller. Thus, mitosis occurs earlier the yeast accomplish their normal size. This suggests that cell partitioning may be regulated in part by dilution of Wee1 poly peptide in cells as they grow larger.

Linking Cdr2 to Wee1 [edit]

The protein kinase Cdr2 (which negatively regulates Wee1) and the Cdr2-related kinase Cdr1 (which directly phosphorylates and inhibits Wee1 in vitro)^[xi] are localized to a band of cortical nodes in the middle of interphase cells. Afterwards entry into mitosis, cytokinesis factors such as myosin II are recruited to like nodes; these nodes somewhen condense to form the cytokinetic band.^[12] A previously uncharacterized protein, Blt1, was institute to colocalize with Cdr2 in the medial interphase nodes. Blt1 knockout cells had increased length at segmentation, which is consistent with a delay in mitotic entry. This finding connects a physical location, a band of cortical nodes, with factors that have been shown to direct regulate mitotic entry, namely Cdr1, Cdr2, and Blt1.

Farther experimentation with GFP-tagged proteins and mutant proteins indicates that the medial cortical nodes are formed by the ordered, Cdr2-dependent assembly of multiple interacting proteins during interphase. Cdr2 is at the top of this hierarchy and works upstream of Cdr1 and Blt1.^[13] Mitosis is promoted by the negative regulation of Wee1 past Cdr2. Information technology has also been shown that Cdr2 recruits Wee1 to the medial cortical node. The mechanism of this recruitment has yet to be discovered. A Cdr2 kinase mutant, which is able to localize properly despite a loss of function in phosphorylation, disrupts the recruitment of Wee1 to the medial cortex and delays entry into mitosis. Thus, Wee1 localizes with its inhibitory network, which demonstrates that mitosis is controlled through Cdr2-dependent negative regulation of Wee1 at the medial cortical nodes.^[13]

Cell polarity factors [edit]

Prison cell polarity factors positioned at the cell tips provide spatial cues to limit Cdr2 distribution to the cell eye. In fission yeast Schizosaccharomyces pombe (South. Pombe), cells dissever at a divers, reproducible size during mitosis considering of the regulated action of Cdk1.^[14] The prison cell polarity poly peptide kinase Pom1, a member of the dual-specificity tyrosine-phosphorylation regulated kinase (DYRK) family of kinases, localizes to cell ends. In Pom1 knockout cells, Cdr2 was no longer restricted to the cell middle, but was seen diffusely through half of the cell. From this data information technology becomes apparent that Pom1 provides inhibitory signals that confine Cdr2 to the middle of the cell. It has been further shown that Pom1-dependent signals pb to the phosphorylation of Cdr2. Pom1 knockout cells were also shown to split up at a smaller size than wild-type, which indicates a premature entry into mitosis.^[13]

Pom1 forms polar gradients that peak at jail cell ends, which shows a direct link between size command factors and a specific physical location in the cell.^[fifteen] Every bit a cell grows in size, a gradient in Pom1 grows. When cells are minor, Pom1 is spread diffusely throughout the prison cell torso. As the jail cell increases in size, Pom1 concentration decreases in the centre and becomes concentrated at cell ends. Small cells in early on G2 which contain sufficient levels of Pom1 in the entirety of the jail cell have inactive Cdr2 and cannot enter mitosis. It is not until the cells grow into late G2, when Pom1 is confined to the jail cell ends that Cdr2 in the medial cortical nodes is activated and able to start the inhibition of Wee1. This finding shows how jail cell size plays a direct role in regulating the get-go of mitosis. In this model, Pom1 acts every bit a molecular link betwixt jail cell growth and mitotic entry through a Cdr2-Cdr1-Wee1-Cdk1 pathway.^[13] The Pom1 polar slope successfully relays data well-nigh cell size and geometry to the Cdk1 regulatory organisation. Through this slope, the jail cell ensures information technology has reached a defined, sufficient size to enter mitosis.

Other experimental systems for the study of cell size regulation [edit]

One common ways to produce very large cells is by prison cell fusion to form syncytia. For example, very long (several inches) skeletal muscle cells are formed by fusion of thousands of myocytes. Genetic studies of the fruit wing Drosophila accept revealed several genes that are required for the germination of multinucleated muscle cells by fusion of myoblasts.^[16] Some of the central proteins are important for cell adhesion between myocytes and some are involved in adhesion-dependent prison cell-to-cell signal transduction that allows for a cascade of prison cell fusion events.

Increases in the size of plant cells are complicated by the fact that almost all plant cells are inside of a solid prison cell wall. Nether the influence of certain plant hormones the cell wall tin can be remodeled, allowing for increases in prison cell size that are of import for the growth of some plant tissues.

Most unicellular organisms are microscopic in size, simply there are some behemothic bacteria and protozoa that are visible to the naked center. (Encounter Table of cell sizes—Dumbo populations of a giant sulfur bacterium in Namibian shelf sediments^[17]—Large protists of the genus Chaos, closely related to the genus Amoeba.)

In the rod-shaped bacteria E. coli, Caulobacter crescentus and B. subtilis cell size is controlled by a simple mechanisms in which cell division occurs after a constant book has been added since the previous division.^{[18] [19]} By always growing past the same amount, cells born smaller or larger than average naturally converge to an average size equivalent to the corporeality added during each generation.

Cell division [edit]

Cell reproduction is asexual. For most of the constituents of the cell, growth is a steady, continuous process, interrupted simply briefly at M phase when the nucleus then the cell separate in two.

The process of jail cell division, called cell cycle, has iv major parts called phases. The first part, called G₁ phase is marked past synthesis of various enzymes that are required for Dna replication. The 2d office of the cell cycle is the S stage, where Deoxyribonucleic acid replication produces two identical sets of chromosomes. The tertiary part is the G_two stage in which a meaning protein synthesis occurs, mainly involving the production of microtubules that are required during the procedure of division, chosen mitosis. The fourth phase, G phase, consists of nuclear division (karyokinesis) and cytoplasmic division (cytokinesis), accompanied by the formation of a new prison cell membrane. This is the physical division of "mother" and "daughter" cells. The M phase has been broken down into several distinct phases, sequentially known as prophase, prometaphase, metaphase, anaphase and telophase leading to cytokinesis.

Cell sectionalisation is more than complex in eukaryotes than in other organisms. Prokaryotic cells such as bacterial cells reproduce by binary fission, a process that includes Dna replication, chromosome segregation, and cytokinesis. Eukaryotic cell division either involves mitosis or a more complex procedure called meiosis. Mitosis and meiosis are sometimes called the two "nuclear sectionalisation" processes. Binary fission is similar to eukaryote cell reproduction that involves mitosis. Both lead to the production of two girl cells with the same number of chromosomes equally the parental cell. Meiosis is used for a special cell reproduction procedure of diploid organisms. It produces iv special daughter cells (gametes) which have half the normal cellular amount of DNA. A male and a female gamete can then combine to produce a zygote, a cell which again has the normal amount of chromosomes.

The rest of this article is a comparing of the main features of the iii types of cell reproduction that either involve binary fission, mitosis, or meiosis. The diagram below depicts the similarities and differences of these 3 types of jail cell reproduction.

Comparison of the iii types of cell division [edit]

The Deoxyribonucleic acid content of a cell is duplicated at the start of the cell reproduction process. Prior to Deoxyribonucleic acid replication, the Dna content of a jail cell can be represented as the amount Z (the cell has Z chromosomes). Later on the DNA replication process, the amount of Deoxyribonucleic acid in the cell is 2Z (multiplication: 2 x Z = 2Z). During Binary fission and mitosis the duplicated Dna content of the reproducing parental cell is separated into 2 equal halves that are destined to finish up in the ii daughter cells. The terminal role of the cell reproduction procedure is cell division, when daughter cells physically separate apart from a parental cell. During meiosis, there are two cell sectionalization steps that together produce the four girl cells.

Later on the completion of binary fission or cell reproduction involving mitosis, each daughter cell has the same amount of Deoxyribonucleic acid (Z) every bit what the parental jail cell had before it replicated its DNA. These two types of prison cell reproduction produced two daughter cells that have the same number of chromosomes as the parental prison cell. Chromosomes duplicate prior to cell division when forming new peel cells for reproduction. Afterwards meiotic cell reproduction the four daughter cells accept half the number of chromosomes that the parental prison cell originally had. This is the haploid amount of DNA, often symbolized as N. Meiosis is used by diploid organisms to produce haploid gametes. In a diploid organism such as the human being organism, most cells of the torso accept the diploid corporeality of Deoxyribonucleic acid, 2N. Using this notation for counting chromosomes we say that human somatic cells accept 46 chromosomes (2N = 46) while human sperm and eggs have 23 chromosomes (North = 23). Humans have 23 distinct types of chromosomes, the 22 autosomes and the special category of sex chromosomes. There are two distinct sex chromosomes, the Ten chromosome and the Y chromosome. A diploid human being jail cell has 23 chromosomes from that person'southward father and 23 from the mother. That is, your body has two copies of man chromosome number 2, 1 from each of your parents.

Immediately after DNA replication a human cell will have 46 "double chromosomes". In each double chromosome there are two copies of that chromosome's DNA molecule. During mitosis the double chromosomes are split to produce 92 "single chromosomes", half of which go into each daughter jail cell. During meiosis, at that place are ii chromosome separation steps which assure that each of the four daughter cells gets 1 re-create of each of the 23 types of chromosome.

Sexual reproduction [edit]

Though cell reproduction that uses mitosis tin can reproduce eukaryotic cells, eukaryotes carp with the more complicated process of meiosis because sexual reproduction such as meiosis confers a selective advantage. Find that when meiosis starts, the two copies of sister chromatids number 2 are next to each other. During this time, there tin be genetic recombination events. Information from the chromosome ii Dna gained from ane parent (red) will transfer over to the chromosome 2 Deoxyribonucleic acid molecule that was received from the other parent (green). Notice that in mitosis the two copies of chromosome number two do non collaborate. Recombination of genetic information between homologous chromosomes during meiosis is a procedure for repairing DNA damages. This process can also produce new combinations of genes, some of which may exist adaptively beneficial and influence the class of development. Withal, in organisms with more than 1 set up of chromosomes at the principal life cycle phase, sex may also provide an advantage because, under random mating, it produces homozygotes and heterozygotes according to the Hardy–Weinberg ratio.

Disorders [edit]

A series of growth disorders tin can occur at the cellular level and these consequently underpin much of the subsequent form in cancer, in which a grouping of cells display uncontrolled growth and division beyond the normal limits, invasion (intrusion on and destruction of adjacent tissues), and sometimes metastasis (spread to other locations in the body via lymph or claret). Several key determinants of cell growth, like ploidy and the regulation of cellular metabolism, are usually disrupted in tumors.^[20] Therefore, heterogenous cell growth and pleomorphism is one of the earliest hallmarks of cancer progression.^{[21] [22]} Despite the prevalence of pleomorphism in man pathology, its role in disease progression is unclear. In epithelial tissues, pleomorphism in cellular size tin induce packing defects and disperse abnormal cells.^[23] Just the consequence of atypical prison cell growth in other animal tissues is unknown.

Measurement methods [edit]

The jail cell growth tin be detected by a diversity of methods. The prison cell size growth can be visualized by microscopy, using suitable stains. But the increase of cells number is commonly more significant. It tin can be measured by manual counting of cells nether microscopy ascertainment, using the dye exclusion method (i.east. trypan blue) to count just viable cells. Less fastidious, scalable, methods include the use of cytometers, while flow cytometry allows combining prison cell counts ('events') with other specific parameters: fluorescent probes for membranes, cytoplasm or nuclei let distinguishing dead/viable cells, cell types, prison cell differentiation, expression of a biomarker such equally Ki67.

Beside the increasing number of cells, one tin can be assessed regarding the metabolic activity growth, that is, the CFDA and calcein-AM measure (fluorimetrically) non simply the membrane functionality (dye retention), but also the functionality of cytoplasmic enzymes (esterases). The MTT assays (colorimetric) and the resazurin assay (fluorimetric) dose the mitochondrial redox potential.

All these assays may correlate well, or not, depending on cell growth weather condition and desired aspects (activity, proliferation). The task is even more complicated with populations of different cells, furthermore when combining cell growth interferences or toxicity.

See besides [edit]

• Bacterial growth

References [edit]

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10. ^ Wee1 mutants of S. pombe take modest cell size and the homologous proteins in humans also regulate cell entry into mitosis; in Lodish HF, Berk A, Zipursky LS, Matsudaira P, et al., eds. (2000). Molecular cell biology (4th ed.). New York: West.H. Freeman. ISBN978-0-7167-3136-eight.
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13. ^ ^{a b c d} Moseley JB, Mayeux A, Paoletti A, Nurse P (June 2009). "A spatial gradient coordinates cell size and mitotic entry in fission yeast". Nature. 459 (7248): 857–sixty. Bibcode:2009Natur.459..857M. doi:10.1038/nature08074. PMID 19474789. S2CID 4330336.
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18. ^ Taheri-Araghi, S; Bradde, South; Sauls, J. T.; Hill, North. S.; Levin, P. A.; Paulsson, J; Vergassola, G; Jun, S (February 2015). "Jail cell-size control and homeostasis in leaner". Electric current Biological science. 25 (3): 385–391. doi:10.1016/j.cub.2014.12.009. PMC4323405. PMID 25544609.
19. ^ Campos, M; Surovtsev, I. V.; Kato, S; Paintdakhi, A; Beltran, B; Ebmeier, S. E.; Jacobs-Wagner, C (Dec 2014). "A abiding size extension drives bacterial cell size homeostasis". Prison cell. 159 (half-dozen): 1433–1446. doi:x.1016/j.prison cell.2014.11.022. PMC4258233. PMID 25480302.
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21. ^ Travis, West.D.; Brambilla, B.; Burke, A.P; Marx, A.; Nicholson, A.G. (2015). WHO Classification of Tumours of the Lung, Pleura, Thymus and Centre. Lyon: International Agency for Enquiry on Cancer. ISBN978-92-832-2436-v.
22. ^ El-Naggar, A.Grand.; Chan, J.C.K.; Grandis, J.R.; Takata, T.; Slootweg, P.J. (2017-01-23). WHO Classification of Head and Neck Tumours. Lyon: International Agency for Enquiry on Cancer. ISBN978-92-832-2438-9. Archived from the original on 2019-ten-31. Retrieved 2019-x-31 .
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Books [edit]

• Morgan, David O. (2007). The cell cycle: principles of control. London: Sunderland, Mass. ISBN978-0-9539181-2-6.

External links [edit]

• A comparison of generational and exponential models of cell population growth
• Local Growth in an Array of Disks Wolfram Demonstrations Project

What Is The Best Explanation For Increase In Size (Growth) In Any Organism?,

Source: https://en.wikipedia.org/wiki/Cell_growth

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