ABSTRACT Living organisms exhibit tremendous diversity, evident in the large repertoire of forms and considerable size range. Scientists have discovered that conserved mechanisms control the

development of all organisms. _Drosophila_ has proved to be a particularly powerful model system with which to identify the signalling pathways that organize tissue patterns. More recently,

much has been learned about the control of tissue growth, tissue shape and their coordination at the cellular and tissue levels. New models integrate how specific signals and mechanical

forces shape tissues and may also control their size. You have full access to this article via your institution. Download PDF SIMILAR CONTENT BEING VIEWED BY OTHERS GROWTH ANISOTROPY OF THE

reproducible morphological patterns, and what mechanisms underlie the diversity of organ size and shape (Fig. 1) have haunted scientists for over a century. From the early observations of

embryology to the quantitative models of systems biology, important discoveries marked the long history of morphogenesis. _Drosophila_ has proven to be a powerful system with which to

elucidate the molecular mechanisms of morphogenesis, identifying the signals that pattern the body plan and characterizing cell mechanics and dynamics underling tissue remodelling. A

principal challenge is to understand within a single mechanistic framework how these patterning signals and cellular responses—such as cell division and cell shape changes—are coordinated in

tissue growth and tissue remodelling. The size and shape of genetically marked clones of cells reflect in miniature the size and shape of the tissue they belong to. Cell division, cell

death, cell shape changes and cell rearrangements are the building blocks on which tissues are shaped and organs are made (Fig. 2). The orchestration of these elementary processes depends on

a constraining genetic programme operating on cell behaviour: for instance, a specific set of signalling molecules, growth factors, promote cell divisions and tissue size, whereas other

proteins control the orientation of cell divisions, oriented cell rearrangements and so on, and hence tissue shape. A surveillance mechanism orchestrates proper tissue size and shape and

involves reciprocal interactions between the cell and tissue scales. When a group of cells dies, compensatory mechanisms controlled at the tissue level ensure that the proper tissue size and

shape are not compromised. The aim of this review is to highlight recent important findings on the mechanisms of tissue growth and shape and to encapsulate them in a single framework of

morphogenesis. We first focus on how cell division and cell death control tissue growth. We then detail how the mechanics of cell shape and division underlie tissue shape. Finally, we

discuss how feedback mechanisms may orchestrate tissue size and shape. TISSUE GROWTH: TO DIE, TO SURVIVE, TO DIVIDE Tissue growth can be best studied in the _Drosophila_ developing adult

tissues called imaginal discs. Imaginal discs are epithelial layers growing from about 40 cells to 50,000 cells in 4 days of continued divisions. Although this massive increase in cell

number and tissue mass is under organismal control as far as the provision of the necessary energy input is concerned, the control of tissue size is intrinsic to the disc. Proper tissue size

is not reached by counting cells: changes in cell size often yield compensatory modifications in cell number, thereby maintaining tissue size1,2. This suggests that tissue dimensions (size

or mass) may be measured. CELL COMPETITION AND APOPTOSIS Tissue-level control of tissue size is manifest in the process of cell competition discovered 30 yr ago3,4, whereby faster growing

cells can out-compete slow-growing cells (Fig. 2c). For example, wild-type clones can take over entire compartments initially occupied by slow-growing cells heterozygous for the _Minute_

(_M_) mutations in genes encoding ribosomal proteins. Myc is another major regulator of cell competition, with as little as twofold changes in Myc expression being enough to trigger

overgrowth of cells and competition with surrounding wild-type cells5,6. The cellular mechanisms underlying competition are only starting to be unravelled. To some extent, fast cells may

compete with slow cells for limited amount of survival signals provided by the transforming growth factor (TGF)-β/BMP (bone morphogenetic protein) molecule Decapentaplegic (Dpp)7. There is

no consensus, however, on the exact importance of Dpp in the competition process5,6. Competition also involves apoptotic elimination of the slow cells and their engulfment by the

fast-growing cells8. The stress-response pathway mediated by Jun N-terminal kinase (JNK)7 and the pro-apoptotic genes _hid_ (also called _Wrinkled_) and _rpr_5,6 were shown to be involved in

the apoptosis of the out-competed cells. The link between cell competition and tissue size is manifest in the following set of experiments: uniform expression of _myc_, where no competition

occurs, causes tissue overgrowth, whereas mosaic expression of _myc_, which triggers competition, leaves size unchanged, indicating that the out-competed cells buffer the overgrowth of

_myc_-overexpressing cells. Consistent with this, mosaic expression of _myc_ results in tissue overgrowth when cell competition is reduced by blocking apoptosis. Another notable observation

indicates that cell competition in a wild-type tissue buffers variations in tissue size5. CONTROL OF CELL DIVISION Control of tissue size also involves a regulation of cell division. Two

remarkable properties of cell division in imaginal discs are that it is random but uniform across the discs and that it ceases uniformly when correct disc proportions are attained. Two

models have been proposed to explain scale invariance in growing tissues. One model emphasizes the role of local communications between cells with different positional values to drive

intercalary growth9. These communications could be mediated by the cell adhesion molecule Fat, an activator of the Hippo pathway that controls cell proliferation (reviewed in ref. 10).

Alternatively, long-range signalling by extracellular morphogens is viewed as the principal determinant of growth11. Morphogens are molecules that form gradients of concentration from a

source and activate different target genes at different concentration thresholds. The morphogen Dpp controls tissue pattern12,13 and tissue growth14,15. Day and Lawrence11 proposed that the

slope of the gradient promotes cell division above a certain threshold. Provided that the addition of new cells decreases the slope of the gradient, growth would arrest when the gradient

becomes too shallow (Fig. 2). Consistent with this, it was elegantly shown that cell division is transiently induced in regions where the slope of the Dpp gradient is experimentally

modified16. Several observations, however, contradict a simple formulation of this model: (1) uniform Dpp expression causes overgrowth; (2) the assumption that the Dpp ligand gradient scales

with the tissue is not experimentally supported17,18; (3) the model fails to account for uniform cell division in the tissue. Thus, additional mechanisms will be required to explain fully

the control of tissue size. As detailed below, the mechanical constraints imposed by tissue growth on local cell division can also be considered in parallel with signalling. Whereas an

increase in cell number drives tissue growth, tissue shape involves changes in cell positions controlled by cell rearrangements and the orientation of cell division. TISSUE SHAPE: ORIENTING

CELL DIVISION AND MOVEMENTS SPATIAL CONTROL OF CELL DIVISIONS A number of mechanisms have been proposed for tissue elongation. It was suggested a long time ago that polarized cell divisions

might be important for morphogenesis in _Drosophila_19 (Fig. 1a, b). However, the major role of polarized cell rearrangements during cell intercalation in vertebrates and invertebrates (see

below) overshadowed this mechanism. As a result, experimental evidence that polarized cell division also has an essential role in plant and animal morphogenesis only accumulated

recently20,21,22,23,24,25,26, with striking examples in _Antirrhinum_ petal morphogenesis21 and zebrafish neurulation24. In _Drosophila_ too, polarized cell divisions occur and participate

in tissue morphogenesis. A detailed analysis of _Drosophila_ imaginal discs showed, for example, that clones of cells grow anisotropically along the axis of tissue growth because cell

divisions are biased along the proximal/distal axis22. Elongation of _Drosophila_ embryonic epithelia is also controlled to some extent by oriented cell divisions26. What controls the

orientation of cell division? Several components of the planar cell polarity pathway (PCP)—that orient other processes such as hairs and cilia—have been implicated. For instance, the cell

adhesion molecules Dachsous and Fat, which orient PCP signalling, are required in the _Drosophila_ wing22. However, core components of PCP signalling (for example, Dishevelled, Frizzled)

have not been implicated in polarized cell division in the _Drosophila_ wing. Note, however, that Frizzled controls orientation of the mitotic spindle during division of the sensory organ

precursor in the _Drosophila_ notum27. Moreover, PCP signalling controls polarized cell divisions in vertebrates. The search for signals controlling oriented cell divisions is thus still

ongoing in _Drosophila_ and other organisms. CELL DIVISION AND CELL SHAPE Changes in cell shape have also been proposed to drive tissue extension. In an epithelial layer cells adopt

characteristic polygonal shapes dictated largely by the interplay between adhesion and cortical tension28. Cell adhesion mediated by cadherins tends to increase cell contacts whereas

cortical tension exerted by the actomyosin network reduces them. This is remarkably illustrated in post-mitotic tissues, such as the pupal _Drosophila_ retina, where differential adhesion

mediated by E- and N-cadherin controls the shape of cone cells29. In pupae, wing cells remodel their irregular contacts to produce a highly ordered hexagonal tiling by a mechanism

implicating E-cadherin trafficking and PCP signalling30. In remodelling epithelia, cells may change shape markedly. Epithelial cell elongation accompanies several tissue extension processes

such as _Drosophila_ dorsal closure31 and imaginal discs evagination32. The underlying mechanisms remain unclear. What is the effect of cell division on cell shape? During division

epithelial cells exhibit a rounder (less polygonal) morphology, but live imaging has shown that cell contacts are not remodelled and daughter cells remain in contact33. This explains the old

observation that clones remain compact in imaginal discs. Defects in the even distribution of E-cadherin after cell division lead to a disruption of cell contacts and to cell scattering34.

Remarkably few constraints on the process of cell division (such as the production of two new vertices at each round of mitosis) conspire to produce a single topological equilibrium with a

majority of hexagons33,35, without assumptions on the mechanics of cell shape28. Heterogeneities in the rate of cell division locally affect the distribution of cell shape. Thus, the shape

of cells in a growing tissue is influenced by cell surface mechanics and by local cell division rates. CELL REARRANGEMENTS AND INTERCALATION Another major mechanism driving tissue extension

is cell intercalation, whereby cells change position by remodelling their adhesive contacts. The evagination of pupal imaginal wing and leg discs, for instance, was proposed early on to stem

from changes in the organization of cell contacts32. Intercalation has been carefully studied during elongation of the embryo, called germband elongation36,37 (Fig. 2d). In this system,

contacts between antero-posterior neighbours shrink (Fig. 2d, red) and new contacts are formed at a perpendicular axis (Fig. 2d, blue). This process does not depend on external forces

exerted at tissue boundaries, but on the local increase in cortical tension imposed by the enrichment of Myosin-II at shrinking junctions36. Adhesion is also probably downregulated, as

Bazooka (also called Par-3)38—a determinant of E-cadherin stabilization39,40—and E-cadherin37 are downregulated in shrinking junctions. Planar junction remodelling and intercalation are

controlled by embryonic polarity36,38,41. Surprisingly, the non-canonical Wnt PCP pathway is not required for cell intercalation during germband extension. The signals orienting cell

rearrangements remain elusive. The proper shaping of a growing organ thus requires that, as new cells are formed, their relative positions be controlled. This is achieved by regulation of

the cell division orientation and of cell rearrangements. Cell division itself and cell mechanics thus underlie important aspects of tissue shaping. A complete understanding of the

coordination of tissue size and shape must integrate the regulation of tissue growth by signalling pathways with the mechanics and dynamics of morphogenesis at the cellular level. FEEDBACK

MECHANISMS COORDINATING SIZE AND SHAPE Cell division and cell growth drive tissue expansion. Yet, attaining the proper tissue size and shape does not simply rely on cell counting. Thus, a

tissue-intrinsic property informs, in return, dividing cells about their division rate, growth or eventual death. Such a feedback mechanism is required to understand growth arrest and tissue

shape. Stochastic fluctuations or persistent variations in growth rate could produce changes of an internal variable (for example, pressure or Dpp activity) that would, in return, affect

growth rate. An inhibitory negative feedback signal can have a stabilizing effect, smoothening fluctuations and providing the system with a dynamic control to ensure homogeneous growth. What

mechanisms could generate a feedback? Two plausible alternatives have been proposed. Local regulation of the morphogen-ligand or activity gradient might be a way. Regions of enhanced growth

could locally reduce the slope of the Dpp gradient, and hence feed back on growth (Fig. 3a). Quantitative analysis of the establishment of the Dpp ligand gradient18,42,43 showed that it

forms on short timescales (minutes) not commensurate with the long timescales (hours) of tissue growth, consistent with the fact that the ligand gradient does not scale with the tissue17.

However, the activity gradient (monitored by phosphorylated Mad or expression of target genes) is clearly influenced by the local tissue growth43. Further tests of this model will thus

require a better characterization of the temporal lag between ligand and activity gradients and of the effect of growth on the latter. The interplay between cell mechanics and the cell

cycle44,45 is another potential way to provide dynamic regulation of tissue growth, as recently suggested in the _Drosophila_ ovary46. Indeed, an inhibition of growth by mechanical

compression (and stimulation by stretch, Fig. 3c) would provide a negative feedback to reprehend heterogeneities of growth. Using quantitative modelling, Shraiman proposed that mechanical

feedback could account for the uniformity of cell division47. Moreover, combining mechanical feedback with the growth-promoting function of a non-scaling Dpp gradient predicts growth arrest

and scale invariance17,48 (Fig. 3d). This opens up new perspectives and prompts a better integration of the cellular and signalling aspects of morphogenesis in fly and other organisms. A

better understanding of the causal relationships between growth and activity gradient dynamics will be important to probe further how morphogens orchestrate size and shape. Whether

morphogens also control cell division orientation and cell rearrangements remains an open and major question to investigate. It will also be important to test the mechanical feedback model:

do stretch and compression influence cell division and survival? Do fields of forces constrain tissue growth in parallel with growth factors? This mechanical feedback could have other

implications on organ shape. It could orient cell division—as was suggested in plants49—or cell rearrangements. These important discoveries in _Drosophila_ should prompt further studies

testing how they apply to size and shape control in mammals. REFERENCES * Neufeld, T. P., de la Cruz, A. F., Johnston, L. A. & Edgar, B. A. Coordination of growth and cell division in

the _Drosophila_ wing. _Cell_ 93, 1183–1193 (1998) Article  CAS  PubMed  Google Scholar  * Weigmann, K., Cohen, S. M. & Lehner, C. F. Cell cycle progression, growth and patterning in

imaginal discs despite inhibition of cell division after inactivation of _Drosophila_ Cdc2 kinase. _Development_ 124, 3555–3563 (1997) CAS  PubMed  Google Scholar  * Morata, G. & Ripoll,

P. Minutes: mutants of _Drosophila_ autonomously affecting cell division rate. _Dev. Biol._ 42, 211–221 (1975) Article  CAS  PubMed  Google Scholar  * Simpson, P. & Morata, G.

Differential mitotic rates and patterns of growth in compartments in the _Drosophila_ wing. _Dev. Biol._ 85, 299–308 (1981) Article  CAS  PubMed  Google Scholar  * de la Cova, C., Abril, M.,

Bellosta, P., Gallant, P. & Johnston, L. A. _Drosophila_ myc regulates organ size by inducing cell competition. _Cell_ 117, 107–116 (2004) Article  CAS  PubMed  Google Scholar  *

Moreno, E. & Basler, K. dMyc transforms cells into super-competitors. _Cell_ 117, 117–129 (2004) Article  CAS  PubMed  Google Scholar  * Moreno, E., Basler, K. & Morata, G. Cells

compete for decapentaplegic survival factor to prevent apoptosis in _Drosophila_ wing development. _Nature_ 416, 755–759 (2002) Article  ADS  CAS  PubMed  Google Scholar  * Li, W. &

Baker, N. E. Engulfment is required for cell competition. _Cell_ 129, 1215–1225 (2007) Article  CAS  PubMed  Google Scholar  * Garcia-Bellido, A., Cortes, F. & Milan, M. Cell

interactions in the control of size in _Drosophila_ wings. _Proc. Natl Acad. Sci. USA_ 91, 10222–10226 (1994) Article  ADS  CAS  PubMed  PubMed Central  Google Scholar  * Saucedo, L. J.

& Edgar, B. A. Filling out the Hippo pathway. _Nature Rev. Mol. Cell Biol._ 8, 613–621 (2007) Article  CAS  Google Scholar  * Day, S. J. & Lawrence, P. A. Measuring dimensions: the

regulation of size and shape. _Development_ 127, 2977–2987 (2000) CAS  PubMed  Google Scholar  * Lecuit, T. et al. Two distinct mechanisms for long-range patterning by Decapentaplegic in the

_Drosophila_ wing. _Nature_ 381, 387–393 (1996) Article  ADS  CAS  PubMed  Google Scholar  * Nellen, D., Burke, R., Struhl, G. & Basler, K. Direct and long-range action of a DPP

morphogen gradient. _Cell_ 85, 357–368 (1996) Article  CAS  PubMed  Google Scholar  * Burke, R. & Basler, K. Dpp receptors are autonomously required for cell proliferation in the entire

developing _Drosophila_ wing. _Development_ 122, 2261–2269 (1996) CAS  PubMed  Google Scholar  * Martin-Castellanos, C. & Edgar, B. A. A characterization of the effects of Dpp signaling

on cell growth and proliferation in the _Drosophila_ wing. _Development_ 129, 1003–1013 (2002) CAS  PubMed  Google Scholar  * Rogulja, D. & Irvine, K. D. Regulation of cell proliferation

by a morphogen gradient. _Cell_ 123, 449–461 (2005) Article  CAS  PubMed  Google Scholar  * Hufnagel, L., Teleman, A. A., Rouault, H., Cohen, S. M. & Shraiman, B. I. On the mechanism of

wing size determination in fly development. _Proc. Natl Acad. Sci. USA_ 104, 3835–3840 (2007) Article  ADS  CAS  PubMed  PubMed Central  Google Scholar  * Kicheva, A. et al. Kinetics of

morphogen gradient formation. _Science_ 315, 521–525 (2007) Article  ADS  CAS  PubMed  Google Scholar  * Bryant, P. J. & Schneiderman, H. A. Cell lineage, growth, and determination in

the imaginal leg discs of _Drosophila melanogaster_ . _Dev. Biol._ 20, 263–290 (1969) Article  CAS  PubMed  Google Scholar  * Reddy, G. V., Heisler, M. G., Ehrhardt, D. W. & Meyerowitz,

E. M. Real-time lineage analysis reveals oriented cell divisions associated with morphogenesis at the shoot apex of _Arabidopsis_ thaliana. _Development_ 131, 4225–4237 (2004) Article  CAS 

PubMed  Google Scholar  * Rolland-Lagan, A. G., Bangham, J. A. & Coen, E. Growth dynamics underlying petal shape and asymmetry. _Nature_ 422, 161–163 (2003) Article  ADS  CAS  PubMed 

Google Scholar  * Baena-Lopez, L. A., Baonza, A. & Garcia-Bellido, A. The orientation of cell divisions determines the shape of _Drosophila_ organs. _Curr. Biol._ 15, 1640–1644 (2005)

Article  CAS  PubMed  Google Scholar  * Ciruna, B., Jenny, A., Lee, D., Mlodzik, M. & Schier, A. F. Planar cell polarity signalling couples cell division and morphogenesis during

neurulation. _Nature_ 439, 220–224 (2006) Article  ADS  CAS  PubMed  PubMed Central  Google Scholar  * Concha, M. L. & Adams, R. J. Oriented cell divisions and cellular morphogenesis in

the zebrafish gastrula and neurula: a time-lapse analysis. _Development_ 125, 983–994 (1998) CAS  PubMed  Google Scholar  * Gong, Y., Mo, C. & Fraser, S. E. Planar cell polarity

signalling controls cell division orientation during zebrafish gastrulation. _Nature_ 430, 689–693 (2004) Article  ADS  CAS  PubMed  Google Scholar  * da Silva, S. M. & Vincent, J. P.

Oriented cell divisions in the extending germband of _Drosophila_ . _Development_ 134, 3049–3054 (2007) Article  PubMed  Google Scholar  * Gho, M. & Schweisguth, F. Frizzled signalling

controls orientation of asymmetric sense organ precursor cell divisions in _Drosophila_ . _Nature_ 393, 178–181 (1998) Article  ADS  CAS  PubMed  Google Scholar  * Lecuit, T. & Lenne, P.

F. Cell surface mechanics and the control of cell shape, tissue patterns and morphogenesis. _Nature Rev. Mol. Cell Biol._ 8, 633–644 (2007) Article  ADS  CAS  Google Scholar  * Hayashi, T.

& Carthew, R. W. Surface mechanics mediate pattern formation in the developing retina. _Nature_ 431, 647–652 (2004) Article  ADS  CAS  PubMed  Google Scholar  * Classen, A. K., Anderson,

K. I., Marois, E. & Eaton, S. Hexagonal packing of _Drosophila_ wing epithelial cells by the planar cell polarity pathway. _Dev. Cell_ 9, 805–817 (2005) Article  CAS  PubMed  Google

Scholar  * Kaltschmidt, J. A. et al. Planar polarity and actin dynamics in the epidermis of _Drosophila_ . _Nature Cell Biol._ 4, 937–944 (2002) Article  CAS  PubMed  Google Scholar  *

Fristrom, D. The mechanism of evagination of imaginal discs of _Drosophila melanogaster_. III. Evidence for cell rearrangement. _Dev. Biol._ 54, 163–171 (1976) Article  CAS  PubMed  Google

Scholar  * Gibson, M. C., Patel, A. B., Nagpal, R. & Perrimon, N. The emergence of geometric order in proliferating metazoan epithelia. _Nature_ 442, 1038–1041 (2006) Article  ADS  CAS 

PubMed  Google Scholar  * Knox, A. L. & Brown, N. H. Rap1 GTPase regulation of adherens junction positioning and cell adhesion. _Science_ 295, 1285–1288 (2002) Article  ADS  CAS  PubMed

  Google Scholar  * Cowan, R. & Morris, V. B. Division rules for polygonal cells. _J. Theor. Biol._ 131, 33–42 (1988) Article  CAS  PubMed  Google Scholar  * Bertet, C., Sulak, L. &

Lecuit, T. Myosin-dependent junction remodelling controls planar cell intercalation and axis elongation. _Nature_ 429, 667–671 (2004) Article  ADS  CAS  PubMed  Google Scholar  *

Blankenship, J. T., Backovic, S. T., Sanny, J. S., Weitz, O. & Zallen, J. A. Multicellular rosette formation links planar cell polarity to tissue morphogenesis. _Dev. Cell_ 11, 459–470

(2006) Article  CAS  PubMed  Google Scholar  * Zallen, J. A. & Wieschaus, E. Patterned gene expression directs bipolar planar polarity in _Drosophila_ . _Dev. Cell_ 6, 343–355 (2004)

Article  CAS  PubMed  Google Scholar  * Harris, T. J. & Peifer, M. Adherens junction-dependent and -independent steps in the establishment of epithelial cell polarity in _Drosophila_ .

_J. Cell Biol._ 167, 135–147 (2004) Article  CAS  PubMed  PubMed Central  Google Scholar  * Pilot, F., Philippe, J. M., Lemmers, C. & Lecuit, T. Spatial control of actin organization at

adherens junctions by a synaptotagmin-like protein Btsz. _Nature_ 442, 580–584 (2006) Article  ADS  CAS  PubMed  Google Scholar  * Irvine, K. D. & Wieschaus, E. Cell intercalation during

_Drosophila_ germband extension and its regulation by pair-rule segmentation genes. _Development_ 120, 827–841 (1994) CAS  PubMed  Google Scholar  * Entchev, E. V., Schwabedissen, A. &

Gonzalez-Gaitan, M. Gradient formation of the TGF-β homolog Dpp. _Cell_ 103, 981–991 (2000) Article  CAS  PubMed  Google Scholar  * Teleman, A. A. & Cohen, S. M. Dpp gradient formation

in the _Drosophila_ wing imaginal disc. _Cell_ 103, 971–980 (2000) Article  CAS  PubMed  Google Scholar  * Chen, C. S., Mrksich, M., Huang, S., Whitesides, G. M. & Ingber, D. E.

Geometric control of cell life and death. _Science_ 276, 1425–1428 (1997) Article  CAS  PubMed  Google Scholar  * Nelson, C. M. et al. Emergent patterns of growth controlled by multicellular

form and mechanics. _Proc. Natl Acad. Sci. USA_ 102, 11594–11599 (2005) Article  ADS  CAS  PubMed  PubMed Central  Google Scholar  * Wang, Y. & Riechmann, V. The role of the actomyosin

cytoskeleton in coordination of tissue growth during _Drosophila_ oogenesis. _Curr. Biol._ 17, 1349–1355 (2007) Article  PubMed  Google Scholar  * Shraiman, B. I. Mechanical feedback as a

possible regulator of tissue growth. _Proc. Natl Acad. Sci. USA_ 102, 3318–3323 (2005) Article  ADS  CAS  PubMed  PubMed Central  Google Scholar  * Aegerter-Wilmsen, T., Aegerter, C. M.,

Hafen, E. & Basler, K. Model for the regulation of size in the wing imaginal disc of _Drosophila_ . _Mech. Dev._ 124, 318–326 (2007) Article  CAS  PubMed  Google Scholar  * Lynch, T. M.

& Lintilhac, P. M. Mechanical signals in plant development: a new method for single cell studies. _Dev. Biol._ 181, 246–256 (1997) Article  CAS  PubMed  Google Scholar  Download

references ACKNOWLEDGEMENTS We thank Pierre Golstein and Steve Cohen for suggestions that improved the manuscript. The hecuit lab is supported by the CNRS, Agence Nationale de la Recherche

and Association pour la recherche contre le cancer. AUTHOR INFORMATION AUTHORS AND AFFILIATIONS * Université de la Méditerranée, Institut de Biologie du Développement de Marseille Luminy

(IBDML),, Thomas Lecuit & Loïc Le Goff * CNRS, UMR6216, Campus de Luminy case 907, 13288 Marseille Cedex 09, France , Thomas Lecuit & Loïc Le Goff Authors * Thomas Lecuit View author

publications You can also search for this author inPubMed Google Scholar * Loïc Le Goff View author publications You can also search for this author inPubMed Google Scholar CORRESPONDING

AUTHOR Correspondence to Thomas Lecuit. ETHICS DECLARATIONS COMPETING INTERESTS The authors declare no competing financial interests. RIGHTS AND PERMISSIONS Reprints and permissions ABOUT

THIS ARTICLE CITE THIS ARTICLE Lecuit, T., Le Goff, L. Orchestrating size and shape during morphogenesis. _Nature_ 450, 189–192 (2007). https://doi.org/10.1038/nature06304 Download citation

* Issue Date: 08 November 2007 * DOI: https://doi.org/10.1038/nature06304 SHARE THIS ARTICLE Anyone you share the following link with will be able to read this content: Get shareable link

Sorry, a shareable link is not currently available for this article. Copy to clipboard Provided by the Springer Nature SharedIt content-sharing initiative