Developmental Explanations.

Synonyms.

Explanations, developmental. Embryological explanations.

Definition.

A developmental explanation explains how a trait came into being through a process starting at the

single-celled stage of the existence of the organism. Since developmentally explaining a trait is an

explanation of its development, hence requires explaining some detail of the developmental processes

which were involved, “developmental explanation” secondarily means the explanation of a particular

feature, moment or process of development itself, for example cell division, apoptosis, specific pattern

formations.

Characteristics.

Development has narrow and large meanings: very narrowly, it is the embryogenesis, i.e. the process

leading from conception to hatching or birth; less narrowly, it means the process leading from the

zygote to the adult form. The larger meaning covers the whole life of the organism, which includes

episodes such as reproduction and senescence (West-Eberhardt 2003, Gilbert 2003). By nature

developmental explanations pinpoint events in the lifetime accounting for an individual carrying a

trait, whereas evolutionary explanations often stand at the population level.

What development explains?

The general explanandum of developmental explanations is twofold: to explain why and how

a zygote develops into an adult type of its species, with its species-typical traits; and to understand

why and how systematic deviations from the normal type occur, which usually concerns “teratology”.

Often, a back and forth move between teratology and normal development characterizes

developmental explanation, because knowing which alterations (e.g. silencing genes; injecting

proteins etc.) produce a specific abnormal development allows understanding what is necessary to

develop the corresponding normal trait; therefore many experimental developmental theorists proceed

by such controlled perturbations of development, at any hierarchical level (genes, cell, tissues).

Developmental explanations target model organisms such as nematodes, sea urchin, frogs,

chicken; through those models they aim at understanding what is common across many species and

clades. Development has many varieties: some species hatch, some have larval stages, some develop

from a unicellular zygote as a sort of bottleneck between generations – whereas others don’t. Lowest

level mechanisms involving genes and gene transcription are likely to be very general across

multicellular organisms; but some higher level traits typical to a clade (i.e. eyes, hearts, etc.) require

targeting an appropriate model organism.

In principle, any trait in an individual organism can receive a developmental explanation.

However, the focus is often put on species(or clades)-typical traits: heart or central nervous system in

vertebrates, tetrapod’s limb, butterflies’ wings stripes, etc. Some theoreticians view the scope of

developmental explanation as in principle limited to species typical traits and the genealogy of a

species type, then of a family type, etc., as in early descriptive embryology. This conflicts with the

core Darwinian idea that variation is proper to species. Inversely, variants in a population can often

be explained by a same core mechanism, whose various outputs depend on the initial conditions, and

which will yield both statistically typical and also eccentrically varying forms (e.g. stripes on

echinoderms). But this idea of a developmental matrix of variation seems not enough to solve the issue

of the individual vs. typical scope of developmental explanations.

Developmental explanations explain the generation of organic form and therefore, given that

individuals of a same species are typically like their parents, contribute to explain the conservation of

form across time. The transmission of traits across generation is “inheritance”; for biologists of the 19.

century, explaining development was supposed to explain inheritance, whereas the Modern Synthesis

(Darwinian) dissociated inheritance (explained by Mendelian transmission of characters from parents

to offspring from development, as the process of growing individual forms. The integration of

mendelian genetics with darwinism from the 1930s underpinned the split between developmental and

evolutionary theories, and the current call for a new synthesis between development and evolution

(Gilbert et al. 1996). In a radical developmentalist perspective, the constancy of the main

developmental processes (and not the transmission of traits) explains the reproduction of form across

generation and then contributes to explain the conservation of form.

Besides physiology - the science of functioning adult organisms - embryology has been

constituted as the science of study of structure and function of developing organisms, including the

function of developmental processes. In this sense, and given that functionality as well as persistent

form metaphysically characterize organisms, their difference exemplified the two poles of biology,

identified in 1911 by E.S. Russell in Form and function: the science of function and the science of

form. Developmental explanations typically instantiate the explanatory style proper to questions about

biological form. Many of the current controversies about the purported absence of development within

evolutionary biology express this conflict between THESE two stances on biology (Amundson, 2005).

Especially, adaptationism in evolutionary explanation neglects the coherence of organismal form (in

favor of explaining isolated traits as optima), whereas developmental explanation aims at accounting

for it.

Alternative epistemological options in developmental studies.

Embryology emerged in a context where debates opposing preformation and epigenesis were salient.

The current idea that genes and epigenetics both contribute to development sounds like a synthesis of

preformationism and epigeneticism. More generally, developmental explanations can be divided into

two styles (often combined): those which pinpoint processes occurring step after step within

development, and those which specify some informational content or specified dispositions present

along development.

Two other general stances in biology have been conflicting within embryology: vitalism and

mechanism. Vitalists hold that development presents us with the clearest expression of vital forces,

what Driesch called “entelechies”, supposed to make sense of the classical sea urchin experiments.

Mechanists claim that physical and chemical forces are alone at work in development, a process on a

par with other chemical processes like fermentation or corruption. Famously, the school of

Entwicklungsmechaniks (Roux, His) in late 1800s studied development by experimental controlled

perturbation, in order to characterize the conditions under which physical processes result in an

embryogenesis. Nowadays, nobody endorses vitalism, yet there is an informal consensus about the fact

that some “emergence” should occur in development, even if what this means is still debated. But

what shaped modern developmental explanations, in its difference with initial embryology initiated by

Wolff (1763) and culminating with Von Baer (1828), is cell theory and Mendelian genetics, cytology

and molecular biology.

Cells, genes and epigenetics.

Elaborated by Schwann, Schleiden and then Virchow in the late 1800s, cell theory rooted the

concepts of embryologists – layers, tissues, organs – within their substrate, namely cells (Mazzarello,

1999). Cell proliferation proved to be the basic operation which underpinned embryogenetic

development as well as reproduction (the zygote results from cells from the mother and the father).

Genes, postulated by Mendelian theory as the bearers of inheritance, turned out to be localized on

chromosomes and finally identified to their material substrate, DNA in 1953. (However, the

ASSUMED identity between genes of molecular biology and THE genes of classical

TRANSMISSION genetics is highly controversial [Moss, 2003]). Genes have then been central both

in evolutionary and in developmental explanations, because they have been seen both as substrate for

inheritance (which pertains to evolution) and as causes of development (as they code for traits). The

extreme view on the role of genes in development consists in claiming that they are a program for

development (or a “recipe”, as Dawkins says), which is undoubtedly the modern form of

preformationism, whereas this has been challenged by recent advances in our knowledge of

epigenetics, as well as by the ongoing understanding that “genes” are much more complex than a mere

linear continuous strain of coding DNA.

Each cell in a eukaryote multicellular organism has the same DNA in its nucleus, which

conditions proteins and then organismal traits. The genesis of the organisms is precisely the process

through which the zygote multiplies and differentiates into various cell types which in their turn

combine into various tissues and organs, stemming from the various layers emerged in the first stage

(blastula) of the process, and then produce organogenesis. Mitosis explains cell multiplication;

however there remains the question of why and how it is the case that, for example, cells in the brain

develop into synapses and neurons whereas cells in the skin develop into epithelial cells; hence

developmental explanations first aim at uncovering the reasons why each cell expresses distinct

genetic resources. Morphogenesis, or pattern formation, assuming cell differentiation, is the second

issue to be solved.

Genes in nucleus are either expressed (active) or repressed. This expression is mediated by

signals from external environment factors, which allow a cell to express the “right” genes in the place

it is, and therefore, produce proteins, change this environment and contribute to the extant signals

around it, so that it will trigger other events of gene expression; reciprocally, this cellular environment

contains products like transcription factors already synthesized by some genes.

Essential in developmental explanation is the identification of episodes of embryonic

induction, where a cell is instructed to a specific cell fate. Identifying morphogenetic fields as set of

cells likely to undergo a specific fate (limb, eye, etc.) is a crucial step in such explanation, even if

morphogenetic fields can be transformed.

The set of non-genetic factors, intra- or extra cellular, which conditions gene expression, is

often called “epigenetic”. Hence epigenetic factors are sought, which are able to switch off and on

genes, while some genes are precisely acting upon other genes (regulatory genes), whereas others are

expressing proteins required in the shaping of the body. Developmental explanations are thereby in

principle multiscale explanations, because causal factors intervene at each level (signals in the tissues,

e.g. gradients of a substance, signals within the cell and genetic instructions, signaling inter-tissues).

A specific set of genes, developmental genes, condition across many eukaryote phyla the

antero-posterior and dorso-ventral axes, as well as many other feature which seemed previously

analogous (such as eyes). Understanding the specific timing of the activation of those genes is crucial

to understand the process of development. Some biologists (e.g. Carroll 2005) would reconcile

evolutionary and developmental perspectives by seeing developmental theory as the genetics and

epigenetics of developmental genes, yet other Evo-Devo scientists (e.g. Newman and Muller 2005)

view this option as still too much gene-centered.

Cascades, signals and networks.

Models of development involve various kinds of informations: instructions coded in genome,

and signals exchanged between cell environments and receptors in cells (Gilbert, 2003). The role of

the latter has been modeled by the “French flag model” proposed by Lewis Wolpert, which provides a

general view on pattern formation (for example, veins in insect wings, cartilages in vertebrate limbs,

etc.) (Wolpert 1994). Cell types develop according to the gradient of a “morphogen“ produced by the

cells, a threshold in the gradient triggering a specific gene expression in some cells, and then a cell

type; the continuity of the diffusion of the morphogen through the gradient translates into the

discontinuity of cell types, the concentration of the product due to its position informs on the cell fates

(Fig.1). This dialectics between genetic instructions and “positional” information provides a scheme of

genes-cells-tissues interaction ruling morphogenesis. Philosophers should note the pervasiveness of a

vocabulary such as: cells interpret, read their position, etc. Even if those words are rather theoretical

reformulations than metaphors, one can still question whether they are reformulated according to a

unique information-theoretical framework.

A developmental explanation therefore can appear as a cascade of events involving signaling,

production of morphogens, expression and repression of gene products. Modeling those cascades and

identifying the morphogens as well as their propagation dynamics and the cells’ receptivity

mechanisms yields an explanation of morphogenesis, exemplified by the emergence of asymmetry in

the heart.

Fig.1 a. The French flag model pattern. 1b. The causal

underpinning of the flag pattern (After Kerzberg and Wolpert 2007).

The non-linear, complex relationships between thousands of regulatory genes in a cell,

transcription factors, and finally a cell lineage involved in morphogenesis are likely to be

mathematically modeled by networks (Davidson 1996). The topology of the network represents the

signaling, inducing, repressing, and expressing pathways, whereas its dynamics captures the variation

in quantitative variables (amount of genes products, etc.) according to some equations (e.g. Michaelis-

Menten, etc.). ), SINCE the initial investigation of the GRN proper to Endo 16 in sea urchins by

Davidson Gene Regulatory Networks (GRN) have proved therefore to be crucially involved in the

formation of patterns during development (Davidson et al. 2003). The networks view is powerful but,

while it avoids a crude idea of a genetic program ran by development, it still gives genes and

transcripts the leading role in developmental processes. An alternative view emphasizes the

fundamental role of a limited set of molecules (e.g. -cadherin) involved in many developmental

episodes and that is pervasive across many clades, finally compacted into developmental building

blocks (DPM, “Dynamical patterning modules”, see Newman and Forgacs, 2005), irrespective of

which genes will be recruited to supervise development. GRN are clearly developmental modules. At

a higher level, endoderm and mesoderm are also developmental modules, as well as Newman’s DPN.

Plausibly, alternative interpretations of developmental explanation –e.g., more or less gene-oriented –

are also distinguishable through the way they identify developmental modules. This is because they do

not use the same criteria to pinpoint them.

Nevertheless, GRN are also likely to account for many features of developmental processes,

especially canalization (because they offer multiple pathways between a given output and input, so

that the failure of some genes does not often affect the final product) and plasticity, two key issues for

Evo-Devo.

Articulating explanatory regimes.

“Developmental explanation” in general means explaining a trait by unraveling a

developmental process. When and how are developmental explanations needed? According to Ernst

Mayr (1961) developmental explanations pertain to proximate causes of phenomena, and evolutionary

explanations to their ultimate causes. However, given that natural selection supposes variation and

that some variation relies upon possibilities given by developmental processes (and not mere

mutations and recombinations), developmental explanations may be implied by evolutionary

questions. In general “developmental constraints” condition the generation of variation, through which

selection shapes traits and organisms. Therefore evolutionary and developmental explanations seem

complementary, the former specifying which variations are available and the second explaining which

actual variants will emerge on the basis of these variations.

However it may be that sometimes a developmental explanation is sufficient because it

unravels a physico-chemical structure involved in a large set of phyla, and therefore explains

the pervasiveness of some traits without a need to appeal to selective pressures. The self-

organising gene networks investigated by Kauffmann’s Origins of Order (1993) provide

developmental explanation of this type. An example would be the modularity of cell metabolic

networks: even if it seems that modularity confers a selective advantage (through robustness),

so that natural selection seems responsible for the fact that all cell types in many clades exhibit

modular networks, the mere topology of networks will indeed promote mostly modular

networks without the need for natural selection to prune a set of randomly varying networks

(Sole and Valverde, 2008). In cases like this, the developmental explanation seems enough to

explain the generality of a trait, without hypothesizing a fixation through natural selection.

The final status of Evo-Devo seems is tied to a decision about whether such cases are

exceptions, or not.

Cross-references.

Model organism; emergence; epigenetics; Gene regulatory network; plasticity; canalization;

evolutionary explanation.

References.

Amundson R. (2005) The changing role of embryo in evolutionary theory. Cambridge: Cambridge

University Press

Carroll S. (2005) Endless Forms Most Beautiful: The New Science of Evo Devo and the Making of the

Animal Kingdom. New-York : Norton

Davidson, E. H. (1986). Gene Activity in Early Development. Orlando, Florida: Academic Press.

Forgacs G. & Newman S. (2005). Biological Physics of the Developing Embryo. Cambridge:

Cambridge University Press.

Gilbert S. (2003) Developmental biology. Sunderland, Sinauer.

Kerszberg M., Wolpert L. (2007) Specifying Positional Information in the Embryo: Looking

Beyond Morphogens. Cell, 130: 205-210.

Mazzarello P. (1999) “A unifying concept: the history of cell theory”. Nature Cell Biology 1: E13 -

E15

Müller G., Newman S. (2005) “The innovation triad: an evo-devo agenda.” J. Exp. Zoo. 304 B 6: 487-

503.

Sole R., Valverde S. (2008) “Spontaneous emergence of modularity in cellular networks.” J. R. Soc.

Interface, 5: 129-133.

Wolpert L. (1994) “Positional information and pattern formation in development.” Developmental

genetics, 15: 485-490.

Definitions

Classical sea urchin experiments in developmental biology.

Manipulations of sea urchins embryo have been important benchmarks in the development of

embryology, after the framework set by the Entwicklungsmechanik (e.g. Roux, His etc.) in the 1890s:

perturbing at various stages the development in order to unravel the mechanisms at each stages of

development. Sea urchins were easy to handle model organisms, even if until Hans Spemann the

embryological techniques were quiet crude.

The first crucial experiment was done by Hans Driesch (1894): a sea urchin, when divided

after the first cell stage (or before the fourth), develops into two sea urchins. The later the stage, the

smaller the embryos. This experiment was, first by Driesch himself, seen as an argument for vitalism

(the vital power being efficient in both embryo; cutting it off should have simply broken a purely

material disposal).

Hans Spemann did two important experiments: in the fist, one half of a blastomere of a sea

urchin develops into a complete one. In the second one, done with Hilde Mangold (1924), a set of sea

urchin cells from an embryo induces Siamese twins when grafted in another urchin embryo (although

not any cut of the urchin leads to this result). This second kind of experiments has been understood as

an argument against preformism. Specifically, it gave an evidence for embryonic induction. Spemann

and Mangold saw as an “organizer” the substance which induces the second sea urchin embryo. More

precisely, because the fate of the transplanted cells could therefore be traced during development,

Spemann and Mangold were able to demonstrate that the graft became notochord, yet induced

neighboring cells to change fates. These neighboring cells adopted differentiation pathways that were

more dorsal, and produced tissues such as the central nervous system, somites and kidneys.

Afterwards, against Spemann’s vitalism, it has been proven that even killed cells from the organizer

substance were able to induce the development, which prevented vitalistic interpretations of the

organizers.

Fig. Spemann Mangold experiment – induction of a Siamese sea urchin embryo by grafting an

extract of the left cell.

Canalization

First recognized by Conrad Waddington, canalization means that many perturbations in the

genes will not change the phenotypic output of the process. Waddington in The strategy of the genes

(1957) used the metaphor of “epigenetic landscapes” (Fig.a), genes being like the nails which hold the

ropes underpinning a valley (Fig. b), in such a way that moving and displacing them does not change

much the general landscape. Canalization occurs also with regard to the environment. Phenomena like

genetic assimilation mean therefore that new channels have been created. Canalization also implies

that organisms with various genotypes may have the same phenotype, which contributes to explain

typicality in various species.

Canalization raises two main sets of question. First, developmental and molecular: what are

the mechanisms underlying it (Masel and Siegal 2009)? Second, evolutionary: given that canalization

means robustness in the face of either mutational or genetic change, one should ask which came first

(Wagner, 2005): has canalization evolved as an adaptation in the face of environmental variations? Or

has it been selected because of the buffering against mutational perturbation (genetic noise)? Lehner

(2010) argued that it is indeed an adaptation for environmental variation, and robustness vs. mutational

robustness is a byproduct.

Besides the evolutionary cause of canalization, biologists also investigate its evolutionary

effects. It has been argued that canalization, as a form of robustness, indeed increases evolvability:

even if it seems to decrease phenotypic variability and then the opportunities for selection, it appears

that canalized developmental systems, because of their robustness across a wide range of variations,

allow more evolution, since genotypic variation can accumulate without hampering the production of a

viable phenotype.

Masel J., Siegal M. (20009) “Robustness: mechanisms and consequences.” Tr. Gen. 25(9): 395–403

Lehner B. (2010) “Genes Confer Similar Robustness to Environmental, Stochastic, and Genetic

Perturbations in Yeast.” PLoS ONE 5(2): e9035

Wagner A. (2005) Robustness and evolvability and living systems. Princeton: Princeton University

Press.

Figure. Canalization (after Waddington). A. Epigenetic landscape, figuring the robustness of

developmental fates. B. Genetic underpinning of canalization.

Preformation and epigenesis

The main alternative about development since the 17 th century opposed preformism and epigeneticism.

Given that to reproduce and grow are properties definitive of living beings, the mysteries of organisms

coming to life have ever been puzzling, and scientists like Aristotle, Descartes or Harvey or Leibniz

suggested theories of development, which already can be ranged along this distinction (Smith, 2007).

Preformism holds that the adult preexists within the first cell, so that development is a mere

unfolding of this preformed germ. Elaborated about 1670-1700 by philosophers (Leibniz,

Malebranche) and scientists who just discovered the use of the microscope (Swammerdam,

Loewenhook), this view denoted first the extreme idea that a whole individual is contained in the germ

as a miniature, an idea later rejected by most thinkers for being too much theologically committed.

Preformism of this kind is famously said to have been refuted by Wolff (Theorie der Generation,

1763) and his description of transforming structures. Yet it can also characterize a view which

emphasizes that something invisible proper to the species type – that late 18 th century scientists like

Haller or Bonnet called “dispositions” - is already effective and active within the first stages of the

embryo (Sloan, 2001). However, modern-day biology often has a very similar use of the concept of

information: as a set of “instructions”, the genome pre-forms the adult organisms.

Epigenesis defines the alternative position, which states that nothing organized exists at the

beginning of the embryo, and that development occurs by the continuous action of forces building step

after step the organism, one layer after the other, with many transient structures which disappear at the

next stage, a fact precluding all initial preformation. Plausibly, scientific embryology began with the

epigenesis defended by descriptive embryology of Caspar Wolff Theoria Generationis (1758) and

Carl Ernst Von Baer’s Entwicklungsgeschichte des Thieres (1829), a universally praised achievement

of embryology. The crucial discovery of embryological layers (ectoderm, endoderm, mesoderm) came

in this framework just after Wolff’s work, by Pander in 1817, with whom embryology extended from

the description of organogenesis to the early embryogenesis. Yet, radical epigeneticism is at pain

explaining why all development in a species in many distinct conditions leads to similar offspring. For

example Von Baer, unlike Wolff, assumed ideal types as the endpoint of embryogenesis, somehow

orienting development, an idea which departs from radical epigeneticism. Historically, as it was

acknowledged by Wolff, epigeneticism came with a belief in spontaneous generations, because both

ideas are committed to a belief in the emergence of organized from non-organized. This commitment

was a main reason for people to be defiant against epigeneticism, or on the contrary, to hold (like the

philosopher Herder, Ideas for a philosophy of the history of mankind, 1807) a wide transformist view

of whole nature from dust to men; however, less radical epigeneticism such as Von Baer’s abandoned

spontaneous generation. Nowadays (Muller and Olsson 2003), molecular biology and genetics

sometimes hold an informational preformism, when they see the genes as the only key for

development. The controversy between preformism and epigenesis is currently cast in terms of the

roles of genes and especially developmental genes in development. The whole developmental process

therefore relies on a dialectical interplay between genes and epigenetics, this last term being either

narrow (cell environment) or large (body environment, such as parents behavior, maternal proteins in

the womb, etc.). The focus on epigenetics in such dialectics somehow follows from the epigeneticist

tradition in embryology.

Müller G., Olsson L. (2003) “Epigenesis and epigenetics.” In Hall B., Olson W. Keywords and

concepts in evolutionary developmental biology. Cambridge: Harvard University Press,

pp.114-123.

Sloan P. (2002) “Preforming the Categories: Eighteenth-Century Generation Theory and the

Biological Roots of Kant’s A Priori.” Journal of the History of Philosophy 40, 2: 229-

253.

Smith J. E. H. (ed.) (2006) The Problem of Animal Generation in Early Modern Philosoph. Cambridge

University Press.

Embryonic induction

Before the rise of genetics, Hans Spemann in 1901 already emphasized the role of inducers at

the tissular scale, a role which can be played by many chemical substances, as Joseph Needham

recognized later (Order and life), leading to the “paradox of an apparently nonspecific stimulus

eliciting a specific developmental response “ (Jacobson and Sater, 1988, 341). Inducers trigger the

development of set of cells, morphogenetic fields, likely to develop into specific cell fates, for

example the neural crest is a transitory structure which among other things gives rise to the nervous

system. Morphogenetic fields can until some stage be induced into other fates by proper induction as it

has been shown by Spemann and Mangold sea urchin experiment. This proves the plasticity proper to

early development.

The experimental investigation of the nature of inducers as well as the relation between

morphogenetic fields and organizers has been a main endeavor of embryology in the pre-molecular

biology era. Current developmental theory investigates the genetic mechanisms of induction in terms

of transcription factors, etc., and the developmental genes such as homeogenes underpinning

morphogenetic fields (De Robertis et al. 1991)

Inducers cannot induce anything except in a “competent” tissue, i.e. which is already prepared

to deal with them and respond to them. This has been again shown about the induction of central

nervous system, which actually involves more requisites than the sole induction by a specific center in

mesoderm – as one usually thought - , but also signals expressed in the ectoderm already from the

blastula stage, without which neural induction is inefficient (Kuroda et al. 2004). Therefore

developmental processes require both induction and “competence” (as a capacity to respond to

specific signals) (Dawid 2004), which is a modern version of the complementarity between epigenesis

(inducers) and preformism (competence) as two poles in developmental explanations.

Dawid I. (2004) “Organizing the Vertebrate Embryo. - A Balance of Induction and

Competence.” PlosBio, 2, 5: 0579-0583

De Robertis E., Morita E., Cho K. (1991) “Gradient fields and homeobox genes.” Development 112:

669-678.

Jacobson A., Sater A. (1988) “Features of embryonic induction. Development 104: 341-359.

Kuroda H., Wessely O., De Robertis E. (2004) “Neural Induction in Xenopus: Requirement for

Ectodermal and Endomesodermal Signals via Chordin, Noggin, b-Catenin, and Cerberus.”

PlosBio. 2, 5: 623-634.

Plasticity

Plasticity means first the ability of some organisms to develop into several possible

phenotypes depending on which environment they face. For instance, crocodiles with a same genotype

will develop either into male or into females depending upon temperature. The phenomenon of

plasticity has always been seen as proper to the living things, and was an important keyword in 18th

Century vitalism. In the era of genetics, plasticity means a one-to-many mapping between genotype

and phenotype.

Second, quite differently it means developmental plasticity, which is the ability of cells and

sets of cell to adopt various cell fates in development, according to the inductions they will receive.

Sea urchin experiments in around 1900 demonstrated this ability, first when a sea urchin embryonic

cell once divided gave rise to two embryos (Hans Driesch) – which proved that embryonic cell were

likely to adopt all fates, i.e. were “totipotent”; second, when Spemann and Mangold established that an

inducer from a sea urchin embryo could induce another a recipient embryo to develop a Siamese

urchin within itself: therefore, cells were plastic because they have shown they could change fate

according to the inducer.

Gerhardt and Kirschner (2005) argued that a form of plasticity proper to the most basic

metabolic mechanisms in cells allowed them to be conserved across phyla and to be recruited in

various clades so that many organizational solutions had been possible on the basis of the same “core

processes” – an important notion of plasticity they called “facilitated variation”.

In population genetics and quantitative genetics, plasticity has often been taken into account in

terms of reaction norms of genotypes. However recent critiques from evolutionary developmental

biology (Evo-Devo) contested this statistical take on plasticity. Other approaches saw plasticity as a

character, in order to ask questions about the evolution of plastic, still a quite controversial view (see

Via, 1993).

The synthesis between evolutionary approaches of plasticity – and then between evolutionary

(or phenotypic) and developmental plasticity – is still on the agenda. Such synthesis is crucial for

understanding the role of development in biology because both require understanding development:

there is plasticity within development – ascribed essentially to cells and cell sets – and then plasticity

as phenotypic plasticity, reached through development, and ascribed to genotypes or organisms. Often,

plasticity is adaptive (West-Eberhardt, 2003), and through it development plays an important role in

evolution, by conditioning the fitnesses of phenotypes of a same genotype. This provides therefore a

major argument for those who claim – against the Modern Synthesis view - that development is

relevant to evolution.

Even if prima facie plasticity means variability and opposes canalization in development or

robustness in general, plasticity may however be seen as a form of robustness, because through change

a developing organism may keep constant some parameters in the face of changing environment

(Sultan & Stearns, 2005).

Kirschner, G. W., Gerhart J. (2005) The Plausibility of Life: Resolving Darwin's Dilemma. New

Haven : Yale University Press.

Sultan S., Stearns S. (2005) “Environmentally Contingent Variation”. In Hallgrimsson, B. & B.K.

Hall (eds), Variation: A Hierarchical Examination of a Central Concept in Biology. New-

York: Academic Press, pp. 303-332.

Via, S. (1993). “Adaptive phenotypic plasticity: target or by-product of selection in a variable

environment?” American Naturalist, 142 : 352 -365.

West-Eberhardt, M. 2003. Developmental plasticity and evolution. Oxford: Oxford University Press.

Developmental modules

Any set of cells, or genes, which is more intrinsically connected than connected to its surroundings,

which is constant across some clades, and which plays a specific causal role in development is a

developmental module. For example endoderm is a developmental module, but also the Gene

Regulatory Network of skeletogenic micromere cell lineage in sea urchins (Oliveri et al. 2008).

Developmental modules are therefore important units of analysis, because they are constant across

many species, and developmental theory is mostly interested in commonalities across phyla (e.g.

regular constant developmental mechanisms such as apoptosis) rather than differences (unlike the

evolutionary viewpoint). They exist at many levels: genetic (GRNs), cellular (morphogenetic fields),

and tissues (germ layers: ectoderm, etc.), and therefore may have some overlap.

Although quasi-independence defines modules in general, developmental modules are not

necessary the same modules as the ones indentified by physiology or morphology (Winther, 2001).

For instance, the mesoderm – a developmental module – gives rise to the heart (a physiological

module), but is also involved in the production of the vertebrate eye (another physiological module).

Modularity seems tied to evolvability (Wagner and Altenberg 1996) because it entails that no

variation in a subpart is likely to change the functioning of the whole, therefore mosaic evolution can

be possible. Developmental modularity fulfils the same evolutionary requirements. It raises the

question of its evolutionary origins: is it given with the first elementary eukaryote, and, basically the

most basic cell mechanisms? Or has it been selected for some advantages, or evolved as a byproduct

of selection for some developmental mechanisms? No consensus is yet attained.

Oliveri P., Tu Q., Davidson E. (2008) “Global regulatory logic for specification of an embryonic cell

lineage.” PNAS , 105,16: 5955–5962.

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Asymmetry of the heart, development.

A developmental explanation appears as a cascade of events involving signaling, production

of morphogens, expression and repression of gene products. Modeling those cascades and identifying

the morphogens as well as their propagation dynamics and the cells’ receptivity mechanisms yields an

explanation of morphogenesis. The embryonic apparition of an asymmetry in the heart results from

such cascade, where each moment of the process involves specific genes and molecules, and where

important structures are often transitory, a crucial fact first emphasized by advocates of epigenesis

such as Caspar Wolff or Carl Ernest Von Baer.

At the venous pole of the embryonic vertebrate heart, a transitory structure, the proepicardium

(PE) produces the epicardium, coronary vasculature, and fibroblasts. In the chicken embryo, the PE

displays left-right asymmetry and develops only on the right side, while on the left only a vestigial PE

is formed, which subsequently gets lost by apoptosis (Shlueter and Brand 2009). This asymmetry

results from a cascade of signaling and gene expression events which involves both sides of the PE,

originally symmetrical (fig. 1). Transitory structures (here PE) proves therefore to be crucial, since the

symmetrical form yields the asymmetrical pattern. When the asymmetric heart is built the PE

disappears by being integrated into the structures built.

The development of the asymmetry of the heart provides a clear example of our knowledge of

specific morphogenesis, its involving various levels of biological hierarchies, and its proper timing.

Schlueter J., Brand T. (2009) “A right-sided pathway involving FGF8/Snai1 controls

asymmetric development of the proepicardium in the chick embryo.” PNAS, 106, 18:

7485–7490

Takano K., Ito Y., Obata S., Oinuma T., Komazaki O., Nakamura M., Asashima M.(2007)

“Heart formation and left-right asymmetry in separated right and left embryos of a

newt.” Int. J. Dev. Biol. 51: 265-272.

Fig.1.The developmental cascade yielding the LR asymmetry of the cardiac venuous pole.