Genes, structuring powers and the flow of informationin living systems

Frode Kjosavik

Received: 6 July 2012 / Accepted: 28 November 2013

� Springer Science+Business Media Dordrecht 2013

Abstract Minimal genetic pre-formationism is defended, in that primacy is ascri-

bed to DNA in the structuring of molecules through molecular codes. This together

with the importance of such codes for stability and variation in living systems makes

DNA categorically different from other causal factors. It is argued that post-tran-

scriptional and post-translational processing in protein synthesis does not rob DNA of

this structuring role. Notions of structuring causal powers that may vary in degree, of

arbitrary molecular codes that are more or less realized, of partial templating and of

genetic information as a subspecies of mechanistic information are brought in to

support this and to rival causal and semantic notions of information. It is concluded

that the primacy of genes in their structuring of molecules goes together with parity

between genes and non-genetic causal factors in regulation of living systems. This is

seen to hold independently of the radical reconceptualization of organism cum

environment that has been suggested in developmental systems theory.

Keywords Parity thesis � Genes � Codes � Arbitrariness � Mechanisms �Information

Introduction: Minimal pre-formationism

The parity thesis, or the claim that genes are on a par with other factors that causally

co-determine life cycles of organisms, is widely discussed in the contemporary

F. Kjosavik (&)

Department of Philosophy, Classics, History of Art and Ideas, Faculty of Humanities, University of

Oslo, Blindern, P.O. Box 1020, 0315 Oslo, Norway

e-mail: frode.kjosavik@ifikk.uio.no

F. Kjosavik

UMB School of Economics and Business, Norwegian University of Life Sciences, P.O. Box 5003,

1432 As, Norway

e-mail: frode.kjosavik@umb.no

123

Biol Philos

DOI 10.1007/s10539-013-9407-x

debate on gene-centrism and genetic information. Unfortunately, the discussion is

sometimes obscured by the fact that different criteria of parity are adopted without

these being explicitly stated. Thus, Ulrich Stegmann brings out seven ways in which

genes can be taken to be on a par with non-genetic factors (Stegmann 2012b),1 and

the analysis is not intended to be exhaustive. Some of the parity claims would seem

to be derived from general views of causality, i.e., from the fact that there is always

interaction between causes, and that includes genetic causes, which act together

with non-genetic causes—or from ‘‘Millean parity’’, i.e., the view that the

distinction between causes and conditions is arbitrary and that material objects

therefore constitute a uniform ontological category. Such construals of parity,

apparently suggested by the very nature of causality, tend to trivialize the matter.

While more or less interesting interpretations of the parity thesis abound, its original

meaning is to be sought within developmental systems theory (DST), or ‘‘develop-

mentalism’’, where it was first put forth as a meta-claim about the scope for according

primacy to genes through any construal of their causal contributions or distinct

character. Susan Oyama is one of the foremost developmentalists, and she intends the

thesis to be a radical claim about ‘‘parity of reasoning’’ when it comes to

conceptualization of factors that affect living systems and the life processes they take

part in. Hence, it is denied that genes have a unique ‘‘controlling’’ or ‘‘informative’’ role,

that they bear ‘‘representations of’’ traits or organisms, that they constitute the ‘‘essence’’

of an organism or a ‘‘potential’’ that is to be actualized (Oyama 2001; Cf. Oyama 2000).

In Griffiths and Knight (1998), the parity thesis has the implication that empirical

differences between genes and other material factors do not justify metaphysical

distinctions that categorize genes as different from all, or even most, other factors.

This is what is labelled the ‘‘no dichotomies’’-view in Stegmann (2012b), but the latter

is spelt out as a specific claim of parity with regard to the status of genes as

‘‘information carriers, replicators and controllers’’, and has ‘‘informational parity’’ as

a special instance. However, the ‘‘no dichotomies’’-view as such can easily be seen to

amount merely to a meta-claim very similar to the one presented by Oyama. I

therefore take the parity thesis in its radical and original form to be a claim about our

conceptual scheme or the ontological commitments that go with it, according to which

genes are not categorically different from other causal factors. To be sure, this is not a

rejection of the idea that there can at some sufficiently fine-grained level be different

categories of causes, where genes make up one of these. Rather, it is a rejection of the

idea that genetic and non-genetic factors are the two fundamental categories of causes

in living systems. Further assessments are needed, then, of which roles of genes are

fundamental enough to potentially make such a categorical difference.2

1 These are ‘‘interactionism’’ (1), ‘‘causal indistinctness’’ (2), ‘‘Millean parity’’, i.e., ontological

uniformity of all causes (3) ‘‘Millean capriciousness’’, i.e., mere interest-relative privileging of causes (4),

the ‘‘no dichotomies’’-view (5), ‘‘informational parity’’ (6) and ‘‘distributive parity’’, i.e., roles had by

genes are had by non-genetic factors as well (7). We shall see that it is 5, 6 and 7 that are most relevant to

developmentalist construals of parity.2 In Weber (2005, 258–263) it is denied that genes are categorically different from other causal factors

because of the metaphysics of causation, i.e., ‘‘no dichotomies’’-parity would seem to follow from

‘‘Millean parity’’.

F. Kjosavik

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Let us call the claim that genes are not categorically different from non-genetic

causal factors that affect living systems a thesis of radical parity. Let radical

primacy be ascribed to genes in so far as they are categorically different. As the

radical parity thesis is presented by developmentalists, it is not only of theoretical

importance but belongs to a research program, and as such it is supposed to provide

empirical research with a new direction and thereby to undermine even the merely

pragmatic privileging of genes.3 This may or may not be consistent with parity in

the sense of ‘‘Millean capricousness’’ (cf. Stegmann 2012b), in that, as an

alternative to pragmatic gene-centrism, instrumental priority may be given either

arbitrarily, as required by this kind of parity, or more selectively to some class of

non-genetic causal factors that are separable from genetic ones.

What underlies the thesis of radical parity would seem to be an attack on genetic

‘‘pre-formationism’’, since it is the somewhat crude idea that an organism is pre-

formed in the genes that has led to the privileging of genes over all other factors

historically. Through genetic pre-formationism, causal priority claims with regard to

replication have been brought together with causal priority claims in development,

and to some extent the latter have even been inferred from the former. Discussions

of parity in specific senses independently of this may turn into discussions of the

distinct character of genes rather than of the genetic primacy issue, and thereby

render the entire discussion of parity uninteresting, in so far as other causal factors

can be seen to have a distinct character as well.

Some version of genetic pre-formationism arguably lingers on in the minds of

many working biologists, as if there are ‘‘traitunculi’’ in the genome (Schaffner 1998).

A ‘‘computer version’’ might even bring in a genetic program that contains at least

some ‘‘traitunculi’’ in its code-script, and thereby yields a high degree of

developmental fixity across a range of normal environments. On the other hand,

Evelyn Fox Keller has argued that if one is to stick to the idea of a program in the

organism, one should speak of a ‘‘cellular program’’ that reads genes as data rather

than of a genetic program with the genes themselves as instructions (Fox Keller 2001,

302–303). Such a shift in locus for the program would indeed rob genes of their

‘‘controlling power’’, but it would still not rule out that there could be ‘‘traitunculi’’ in

the genome in the form of data to be read by the cell for specification of traits.

Developmentalists would therefore not be satisfied with this proposal either.

There would seem to be two different, very general primacy claims for genes,

then, that developmentalists intend to deny through their radical thesis of causal

parity. Firstly, there is the claim that genes control the organism by regulating living

systems and their development. In general, if x regulates y, it implies that y can be

in different states and that x makes a difference with regard to which state y is in.

Regulatory proteins, hormones and epigenetic marks are examples of factors that

take part in such state modification. What is regulated might be a living system or

any subsystem or component thereof. If it is claimed that there are genetic

instructions and a genetic program for such regulation, that would suggest that

genes are categorically different in their regulatory role. Let us call such a claim of

3 Cf. Griffiths and Gray (2001, 214–215). Godfrey-Smith (2001) distinguishes between ‘‘DST as research

program and as philosophy of nature’’.

Genes, structuring powers

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categorical difference or dichotomy between genes and non-genetic factors, be it

phrased in computer language or in a different way, a claim of radical primacy in

regulatory role, and its negation a claim of radical parity in regulatory role. The

fact that even the subsystems of replication and translation of genes are regulated by

non-genetic factors, like regulatory proteins, or the fact that genes must be re-

conceptualized so liberally as to include widely different causal factors if this is not

to be the case, might be taken by developmentalists as sufficient justification for a

thesis of radical parity in regulatory role.

Secondly, there is the claim that genes specify the structure and traits of an

organism. If x specifies an entity y, it implies that y does not already exist and that the

very structure of y, like the structure of a protein, derives from x, or that y as an

instance of a phenotypic property derives from x. If it is claimed that genes constitute

the data to be read by a cellular program, it suggests that genes are categorically

different in their specifying rather than regulatory role. Let us call such a claim of

categorical difference, be it phrased in computer language or in a different way, a

claim of radical primacy in specifying role, and its negation a claim of radical parity

in specifying role. The fact that it is highly problematic to speak of genes as coding for

phenotypic properties in general might be taken by developmentalists as sufficient

justification for a thesis of radical parity in specifying role. The radical parity thesis is

thereby split into two theses that are independent of each other. While it cannot be

ruled out a priori that there could be other roles than a specifying or regulatory one that

could potentially make a categorical difference between genes and non-genes, these

are arguably the two fundamental roles that are targeted through developmentalist

anti-preformationism, i.e., pre-determination of structure and of processes. At least

one of these theses must be false, then, if genes are to be categorically different from

non-genes in the intended sense.

It should be clear by now that developmentalists are not simply offering a blanket

denial of any special role for genes to play, as implied by ‘‘causal indistinctness’’ in

Stegmann (2012b), i.e., the view that ‘‘genes and non-genetic factors (…) do not differ

in their (causal) contributions to development’’ or as implied by ‘‘distributive parity’’

in Stegmann (2012b), i.e., the view that ‘‘every kind of contribution made by a gene is

also made by some non-genetic factor, and vice versa’’. Rather, developmentalists are

claiming that those kinds of roles that would justify attribution of radical primacy to

genes if had by genes only are also had by non-genetic factors. Regulatory and

specifying roles are of that fundamental kind, unlike, say, enzymatic roles, and there

may be roles had exclusively by genes that still do not privilege genes.

The best defence of radical primacy in terms of either regulation or specification

might lie in an informational role for genes. However, the notion of causal

information is widely taken to be symmetrical between genetic and environmental

factors, which can both be said to carry such information, and even symmetrical

between genes and phenotypic properties, or instances thereof, which can again both

be said to carry such information.4 The notion of intentional information, on the

4 In Bergstrom and Rosvall (2009) it is argued that causal information in Shannon’s sense is of a special

kind that is only carried by a system for transmission, designed by humans or by natural selection, for

efficient packaging, i.e., ‘‘information in the transmission sense’’. It is not clear, though, why information

carried by such a system should be different in kind from correlational causal information in general.

F. Kjosavik

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other hand, is widely considered to be asymmetrical.5 By way of such information,

genes might be conceived of as being in control of an organism as well as

containing specifications of its traits. After all, intentional information in some sense

is the closest we get to attribution of a ‘‘mind’’ to mindless natural processes, i.e., of

controlling power and specifying intentions in a naturalized sense. Primacy in both

regulatory and specifying role would follow, then. However, in her consistent

developmentalism, Oyama insists on the ontogeny of information as well, and

thereby on radical parity in both regulatory and specifying roles.

I shall argue against this claim of ‘‘ontogeny’’ of information, which would seem

to rule out even minimal pre-formation through templating of proteins, thereby

suggesting that there is no sense whatsoever in which there is anything that is

genetically pre-formed in the zygote.6 For this purpose, I shall develop the idea of

sequence-specification by way of structural information. The theoretical framework

for this information concept is based on a novel proposal in Bogen and Machamer

(2011) concerning a special subclass of mechanisms that are said to carry

information of a mechanistic kind. Recently, Kenneth Waters has revived Francis

Crick’s idea of sequence specificity, and argued that genes are different because

they are ‘‘causally specific’’ or fine-tuned actual difference-makers (Cf. Waters

2007). However, Waters takes sequence specificity with regard to genes to be shared

by spliceosomes, whereas I shall argue that the partial or full templating that goes

with structural information is not to be shared by splicing agents in this way.

No unique controlling role will be attributed to genes, though, as the traditional

genetic pre-formationism would have it—not even in the form of ‘‘sequence

control’’, as suggested by Stegmann, who assimilates genetic causation in some

molecular processes to the sequence control in music boxes, automatic looms and

punch card machines (Cf. Stegmann 2012a). Rather, it will be argued that primacy

in sequence-structuring role goes together with parity in regulatory role, as

regulating power is shared by non-genetic factors even in replication and protein

synthesis.

From molecular codes to structuring powers

Code-talk is not an arbitrary way of insisting on genetic primacy but a way of

characterizing very stable geometrico-mechanical and electro-chemical correlations

in living systems.7 As long as the question of parity is that of whether a class of

molecules that fall under the molecular gene concept is categorically different, we

need not come up with a precise definition of ‘‘gene’’ for the purposes of the

discussion of radical parity. The candidate for radical primacy are structuring

molecular stretches, and these should therefore at least fall under the molecular

5 Cf. Sterelny and Griffiths (1999), 104–105, on the distinction between causal and intentional

information.6 Cf. Godfrey-Smith (2001, 290–295), on the ‘‘extreme anti-preformationism’’ of DST.7 In Machamer et al. (2000), four types of ‘‘bottom out activities’’ are distinguished: (1) geometrico-

mechanical; (2) electro-chemical; (3) energetic; (4) electro-magnetic (p 14).

Genes, structuring powers

123

concept of a gene as this has been applied in claims of parity or primacy. DNA

stretches that ‘‘code for’’ functional RNA stretches, like ribosomal and transfer

RNAs, or for proteins, are to be considered as genes, even if only in a ‘‘split

version’’, because of the introns.8 The coding DNA stretches are themselves always

structuring, then, in so far as the very coding is the structuring.

Not all ‘‘code-talk’’ warrants ascription of sequence-structuring role and power to

genes in the required sense. DNA stretches are often said to ‘‘code for’’ phenotypic

properties in general.9 But this is a sense of ‘‘code for’’ in which environmental factors

can be said to ‘‘code for’’ phenotypic properties as well. In this case, the phrase ‘‘code

for’’ belongs merely to the metalanguage of the biologist, even if the DNA code as

such does not, and it does not correspond to anything deeper than causal difference-

making. It would be better, then, to speak of genes ‘‘for’’ phenotypic differences as

well as environments ‘‘for’’ phenotypic differences, and omit the ‘‘code’’ part of

‘‘code for’’. This parity in difference-making does not necessarily support radical

parity, though, since the categorical difference between genes and other causal factors

may lie at the specific level of sequence-structuring, as I shall argue.

When ‘‘code’’ is taken in its proper sense, as in semiotics and linguistics, there

are at most codes at the molecular level. Even this is often dismissed in the case of

protein synthesis because of all the RNA-intervening factors downstream of the

activation of DNA stretches. To circumvent this problem, we may first define

molecular codes at an abstract level, i.e., in terms of abstract molecule types rather

than concrete tokens, and mappings, or mathematical functions, between these, as

opposed to causal relations. We may then ask to what degree these abstract codes

are realized or instantiated in the concrete, and even whether any ‘‘code talk’’ about

organisms is bound to be merely metaphorical or fictional.10 Those who hold the

latter might just take ‘‘code’’ in my discussion as shorthand for properties of

compositionality, permutability and mapping that are realized to a higher or lower

degree, or more or less fully, at the level of molecular processes in living systems.

We must distinguish between codes that are merely ‘‘combinatorial’’, or, rather,

compositional and permutational, like the DNA system itself as a quaternary code

with four DNA bases, and codes that consist in mappings between systems, where

causal factors ‘‘code for’’ their effects in the proper sense of ‘‘code for’’. In DNA

and RNA stretches, there can be mutations or intersubstitutions in one position

independently of bases in neighbouring positions with the mechanisms of

transcription and translation intact, and this is a very good reason to ascribe DNA

and RNA codes to living systems in the first place. This kind of independence from

immediate context and free permutability is highly atypical of electrochemical

processes in general.11

8 In RNA viruses, RNA takes over the role of DNA in the molecular codes.9 For a criticism of this, see Godfrey-Smith (2000) and Kjosavik (2007).10 For a rich historical account of the emergence of what is taken to be code and information metaphors

in biology, see Kay (2000). Cf. also Levy (2011), where it is argued that code-talk and information-talk

are ‘‘liminal fictions’’ in biology, but that they still have important theoretical roles to play.11 For a precise analysis of this, see the distinction between external and internal ordering in Stegmann

(2012a).

F. Kjosavik

123

The special case of a correspondence between two combinatorial codes, like the

mapping between the DNA and RNA bases as well as the mapping between RNA

base triplets and amino acid residues, is what I shall dub a structuring code. In a

structuring code, there is pattern congruence between the encoding and the encoded

system. The correspondences may be either one–one or many-one, i.e., degenerate

codes are included, as when two different RNA codons code for the same amino

acid. A structuring code is modular, i.e., it has discrete compositional units that are

permutable, like DNA bases, RNA bases or base triplets and amino acid residues.

These modular units therefore make up not only a modular pattern of organiza-

tion—a pattern displayed even by the organelles of a cell—but also a modular, and

thereby language-like, pattern of transmission from encoding to encoded

structure.12

There is an important difference, then, between discrete or digital structuring,

which is encoding in the proper sense, and continuous or analogue structuring,

which is not, and this difference is there even with regard to genetic pre-formation

of proteins. Thus, let us distinguish between the digital and the analogue structure of

a molecule, or of a non-branching molecular subunit. By the former, I shall

understand its discrete, combinatorial structure, i.e., a linear sequence of molecular

subunits, and by the latter, its non-combinatorial structure. The amino acid sequence

that makes up the primary structure of a protein—or of a polypeptide subunit—is

thus the digital protein structure, as opposed to its higher order analogue structure of

coils and folds. Even the DNA and RNA molecules of course have an analogue

structure—which is usually a double or simple helix, respectively—but sequences

of DNA base triplets or RNA codons do not.

Whenever we speak of a genetic code for proteins, we should bear in mind that it

is just a code between the digital structure of DNA or RNA on the one hand and the

digital structure of proteins on the other, i.e., between base sequences and sequences

of amino acid residues—there is no code between the three-dimensional shapes of

full-fledged molecules. This again shows the limits of the genetic pre-formationism

in question, since it is at most the primary protein structure that can be said to be

‘‘pre-formed’’, and not the higher order structure. To be sure, there are also

instances of ‘‘whole structure’’ pre-formation in organisms.13 Thus, cellular

structures serving as ‘‘blueprints’’ for replicate structures in cell division, as in

epigenetic structural inheritance, is a higher-level analogue counterpart to digital

structuring. There is some scope, then, for analogue pre-formation, and for the

exercise of structuring power without a structuring code and unit-by-unit

transmission. But this is the kind of specification of organizational patterns that is

accepted by developmentalists as part of the ‘‘self-structuring’’ of cells. It is

inseparable from a dynamic process where a mother cell is gradually transformed

into two daughter cells. The entities in question are not templating through

independent principles for their own organization, as the strict pre-formation of

12 Cf. the distinction between ‘‘modular’’ and ‘‘holistic’’ transmission in Jablonka (2001, p 105). Cf. also

Jablonka and Lamb (2005).13 There may be ‘‘fragmentation’’ of the whole, though, ‘‘followed by growth, as in a crystal’’. (Cf.

Jablonka 2001, p 105.).

Genes, structuring powers

123

genetic pre-formationism requires. It is digital pre-formation, or sequence-specifi-

cation through molecular codes, that will concern us here, then.

The replication code consists in a sequence complementarity mapping between

the DNA bases, i.e., A ? T, G ? C, T ? A and C ? G. It is a mapping of the set

of units of a combinatorial code onto itself, then. It is realized through causal

correlations between the sequence of DNA bases on one strand of DNA in the

mother cell and the sequence of DNA bases on one strand of DNA in the daughter

cell. Derivatively, there is also an identity code between sequences of complemen-

tary base pairs in double-stranded DNA. Such an identity mapping is a limit case of

a code, based on sequence properties alone, and though it gives rise to a duplicate

molecule, it should not be confused with analogue structuring of a daughter

molecule on the basis of the whole structure of the mother molecule. The replication

code is fully realized in the concrete, i.e., to such an extent that deviations from it

can only be considered as ‘‘copying errors’’, just as there may be errors in the

substitution deciphering of a man-made Morse code.

The transcription code consists in the correspondence between DNA and pre-

mRNA, again by way of a sequence complementarity mapping, namely, A ? U,

G ? C, T ? A and C ? G. The translation code consists in a correspondence

between mature mRNA base triplets and amino acid residues that make up the

primary structure of a protein, by way of specific enzymatic assignment rules, like

AUG ? Met or GGA ? Gly, i.e., mappings onto the amino acids methionine and

glycine, respectively. This presupposes that a ‘‘reading frame’’ is imposed upon the

mRNA transcript, since the latter does not have the higher order organization into

triplets, including start and stop codons, as such. While the translation code itself is

normally considered as ‘‘the genetic code’’, the genetic code is more properly

considered as the transcription code put together with the translation code, at least if

it is to make sense to speak of genes, in the form of DNA stretches, as coding for

RNA or proteins. I have analysed each of these codes and some of the complexities

involved elsewhere (Cf. Kjosavik 2007).

Both the combinatorial codes as well as the replication and transcription codes

are realized, and even the translation code is realized to a high degree in

prokaryotes. The very step of maturation from pre-mRNA to mRNA does not affect

the transcription code between DNA and pre-mRNA, nor does it affect the

translation code between mRNA and proteins. To be sure, the genetic code in the

sense of a code composed of the transcription and the translation code is only

partially realized as such, except in prokaryotes. But the sequence-structuring role

of genes in protein synthesis does not hinge on there being an almost totally realized

genetic code between DNA stretches and amino acid chains. It suffices that both the

transcription stage and the translation stage are determined in accordance with a

code to a high degree, and that the translation stage is determined to a high degree

by the transcription stage.14

14 It might even be suggested that the further processing of the transcript is part of the ‘‘code’’ itself when

the latter is taken in the extended sense of ‘‘coding apparatus’’ rather than in the strict sense of

compositionality, permutability and mapping. But it is the pre-formative power of the genetic code-script

itself by way of pattern congruence that we are after here.

F. Kjosavik

123

The sequence-structuring role of DNA, then, by way of structuring codes, is that

of original sequence-specification in the processes that are patterned by these codes,

whereas that of the RNA transcript is that of derived sequence-specification.

Reverse transcription, where RNA templates DNA, constitutes an exception to this,

but again the further downstream effects of such transcription derives from normal

transcription and should therefore be ascribed to the structuring role and power of

DNA rather than RNA. In general, then, DNA stretches specify RNA stretches,

which may in turn, together with a ‘‘reading frame’’, specify amino acid chains. The

structuring power of DNA reaches throughout transcription and translation, i.e., it is

more far-reaching than that of RNA because it is original to the processes of

transcription and translation, and it is therefore also pre-formative in the required

sense of pre-formationism.15 In RNA splicing and editing, there is no sequence-

specification as such but rather sequence-modification. The RNA transcript may

thereby specify a different amino acid chain, but the processing and editing factors

are not themselves templating but rather modify a template that is already there.

Sequence-specification and sequence-modification are two different ways in which

molecules have a sequence-structuring role and structuring power. Post-translational

protein-splicing is similarly sequence-modifying rather than sequence-specifying.

In addition to a sequence-structuring role, DNA itself also has a regulatory role to

play, in that stretches of DNA modify the states of other DNA stretches, i.e.,

whether they are to be activated, i.e., transcribed or not, or the rate of transcription.

DNA thereby has a regulatory role that is different from its sequence-structuring

role. However, this role does not set it apart from other factors that regulate,

including epigenetic factors, like those involved in DNA methylation and histone

modifications.

To be sure, even epigenetic factors have a structuring power, in addition to their

regulatory power. This is so since in DNA methylation, patterns of methylated and

non-methylated states are themselves replicated onto the DNA strands of the

daughter cells, by way of methyltransferases. A methyl mark or lack thereof on CpG

doublets constitutes a simple binary combinatorial code, and there is also a

correspondence code in replication, which is an identity code between patterns of

methyl marks. There could in principle also be a combinatorial code of histone

modifications, with patterns of histone marks as well as a correspondence between

these in replication that would again be an identity code. However, it is less clear

what are the mechanisms of mitotic inheritance in this case.16 Like a first order,

genetic replication code, a second order, epigenetic one is a source of both stability

and variation. It remains a fact, though, that only DNA, and derivatively RNA, has

first order sequence-structuring roles and powers.

Molecular templates based on a first order structuring code are always arbitrary,

either in the weak sense that the coding principle they are based on could have been

different, i.e., the replication and transcription codes could have been based on a

15 Let us just make use of an intuitive notion of ‘‘causal reach’’ here. Below, it will be made slightly more

precise in terms of flow of ‘mechanistic information’.16 Cf. Zhu and Reinberg (2011) on ‘‘templated modification copying events’’ versus ‘‘modification

reinforcement’’.

Genes, structuring powers

123

different principle than that of sequence complementarity, or in the strong sense that

specific enzymatic assignment rules could have been different, as in the translation

code (Cf. Kjosavik 2007; Stegmann 2004). The correspondence between mother

cells and daughter cells is not arbitrary in this way but is just based on shapes that

take part in a dynamic process of cell reproduction. Arbitrariness requires a sharp

separation between patterns to be mapped onto each other and the very mapping

between these that is not there in the process of reproduction of cellular structures in

general. This arbitrariness is closely linked to the permutational potential of the

molecular codes and thereby to the scope of variation in protein functions. Only a

modular code, with the arbitrariness that goes with it, can support the robustness of

entities as opposed to that of processes, and it is the former that is required by

minimal genetic pre-formationism. Genetic structures are pre-formative in the

primary sense by way of the replication, transcription and translation codes, whereas

epigenetic, higher order ‘‘superstructures’’ are pre-formative in a secondary sense.

From structuring codes to mechanistic structural information

Let us now bring in a notion of information that does justice to the first order pre-

formative or templating role of DNA in a way that developmentalist construals of

information as ‘‘holistic’’ and ‘‘ontogenetic’’ cannot do. Developmentalists empha-

size stable processes over stable entities in living systems—though the former may

have pre-formative analogue templates as integral parts, as in structural inheritance.

Neumann-Held’s proposal of a ‘‘process molecular gene concept’’ (Cf. Neumann-

Held 2006) is still troublesome, though, because it understates the point of minimal

pre-formation or structuring by way of digital templates, which rely on independent

principles for their organization, i.e., on structuring codes. No sharp line can be

drawn between what belongs to a process molecular gene concept and what does

not. On the other hand, there is a sharp distinction between causal factors that are

digital templates and those that are not.

Indeed, living systems as we know them depend on digital pre-formation

throughout the life cycle and in the reproduction of life cycles. What is needed is

therefore a notion of information that can account for such templating, and which is

not just tailored to fit this kind of transmission in particular. The notion of

mechanistic information introduced by Peter Machamer and Jim Bogen, if not fully

developed as such, is a more general notion of information, and one that is intended

to accord well with how working biologists actually speak of information. It is just

of the kind that is needed to account for the fact that DNA exercises a structuring

causal influence despite all the intervening processing in the form of RNA editing

and processing. Partial templating in protein synthesis is thereby captured in a more

precise manner, which also brings it together with full templating as a limit case in

replication.

In general, then, for there to be flow of mechanistic information, an initial cause,

i.e. an entity or activity with causal influence at the initial state, must reach

continuously throughout the entire process to the final state. For this to make sense,

it is necessary that the mechanism have multiple stages of operation. Bogen and

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Machamer distinguish between strength of influence and independence of influence.

These concepts are not worked out in any detail but they are still sufficiently

suggestive for our purposes. The strength of influence of an initial cause depends

upon how many routes to alternative final states that are ruled out or rendered

improbable by it (2011, 851). I take it that in the case of protein synthesis, there is

strong causal influence from DNA to the extent that there are limits to how much the

outcome is modified through intervening factors in transcription and translation,

where these factors are themselves considered as parts of the mechanisms in

question. More precisely, strength would seem to amount to degree of causal

specificity. The independence of influence of an initial cause is determined by the

extent to which the final state depends on background conditions ‘‘over which it has

no control’’ rather than on the initial cause (2011, 851). It is also said to be a

‘‘robustness condition’’. I take it that in the case of protein synthesis, the point is that

it can take place in the face of a wide range of variation in background conditions

outside those of the mechanisms of transcription and translation themselves. The

reach of an initial cause is then defined by ‘‘how many steps are strongly influenced

by it and how independently it influences them.’’ (2011, 852) Alternatively, we

might say that the reach of an initial cause is determined by its degree of causal

specificity and its robustness over multiple stages of operation of a mechanism.

The Krebs or citric acid cycle is considered to be a mechanism that lacks the

required continuity from an initial cause that reaches over its stages of operation to

an end product. An oxaloacetate molecule of the initial state of a Krebs cycle does

not reach throughout the cycle. Rather, what is formed at one stage is just a substrate

for the next stage independently of previous stages, and there are other kinds of

molecules that do not originate in the cycle that are essential to what is formed at

some of the stages.

Protein synthesis, on the other hand, is a process where there is flow of

mechanistic information from initial DNA to amino acid sequence in a protein

precursor. The continuity of the causal reach of the DNA sequence, i.e., its causal

specificity and robustness, is in this case upheld by the transcription and translation

codes. Thus, while all mechanisms display productive continuity, for the

mechanism to carry mechanistic information, an initial cause must reach

throughout the stages of the operation to the very end product. In addition, Bogen

and Machamer require that the latter must play a ‘‘teleological role’’, i.e., the

continuity must be supported by a teleological structure of the proper kind. The

Krebs cycle does not fulfil this condition, i.e., the causal role of the cycle is not

served merely by the ‘‘end product’’ of the cycle but rather by products formed at

various stages. The causal role of protein synthesis, by contrast, is served precisely

by its end product.

The complexities involved in the processes of transcription and translation in

eukaryotes have already been brought up, including alternative splicing, post-

transcriptional editing and post-translational modifications. These complications

undermine any simple idea of ‘‘pattern replication’’, or full templating, in the very

protein synthesis, as Bogen and Machamer point out (2011). More precisely, they

affect the strength of the causal influence exerted by DNA, or its causal specificity

over multiple stages, within these mechanisms. By comparison, I take the process of

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DNA replication, be it in prokaryotes or eukaryotes, to be based on a very strong or

very specific causal influence from mother to daughter DNA, since no intervening

sequence-modifying factors are at work in a mechanism for replication but at most

proof-reading and error-correcting ones.

Still, even in the case of transcription and translation in eukaryotes, the final

protein product is arguably within the reach of the causal influence or the robust

causal specificity of the initial DNA. We can no longer conceive of this as simply a

pattern being ‘‘replicated’’ from DNA to protein in its entirety and in accordance

with a reading frame. But DNA exercises a structuring power by way of coding or

templating steps and thereby reaches throughout the entire process of protein

synthesis. This is so even in the extreme case of the Dscam gene in the fruitfly,

which is often used to discredit even minimalist genetic pre-formationism. The

Dscam gene may give rise to as many as 38016 different proteins through

alternative splicing, which is of course quite remarkable. Nevertheless, it remains a

fact that these proteins make up a family of isoforms that are actually quite

structurally similar to each other. The proteins have only 4 variable domains,

whereas 20 out of 24 domains are the same in all the isoforms. This shows that even

in the case of extensive intervention by sequence-modifying factors, the structuring

power of genes does reach throughout the process of transcription and translation,

from molecular gene to primary protein structure. Structural mechanistic informa-

tion is thereby transmitted through fixed reading frames and sequence-specifying

stretches of the initial pattern that are indeed ‘‘replicated’’ and therefore constant

across protein isoforms.

Furthermore, as required above, mechanistic information is not merely an ad hoc

construal of biological information that is tailored to apply to genes in particular.

After all, even regulation may take place by way of mechanistic information, as in

signalling. However, templating and signalling remain different kinds of processes,

and structural and regulatory mechanistic information ought therefore to be

considered as two different subspecies of mechanistic information. Signalling has in

common with protein synthesis that it is a process where a far-reaching influence of

an initial cause ensures a productive continuity in stages of operation of a

mechanism that also has the proper teleological structure.17 Still, there is no

transmission of a pattern by way of a structuring code, i.e., what is transmitted is not

information about an extensive whole, organized into discrete modular parts, that is

to be partly or wholly preserved across various material substrates through distinct

mapping stages, as in protein synthesis, but a regulatory signal with a certain

intensity, carried serially, in part by way of signal molecules, like hormones,

pheromones and neurotransmitters, and partly by way of cascades through which the

signal is amplified. The latter process thereby also has another teleological role than

the former.

17 In Bogen and Machamer (2011), the case of neurotransmission of a leech reflex is brought up as an

example of a mechanism that carries information, but they do not discuss signalling and signal

transduction in general.

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123

From genetic causation to information and control?

We have seen, then, how structuring power through structural mechanistic

information distinguishes genes from other causal factors and makes them

categorically different, thereby undermining the ‘‘no dichotomy’’ parity in the

unrestricted sense intended by developmentalists as well as any sweeping claim of

distributive parity. Mechanistic information is shared with signal molecules, so

there is still informational parity between these and genes, but signal molecules are

not pre-determinative as such but subservient to processes of regulation. Further-

more, a sequence-specifying role and power of DNA templates is shared with RNA

templates and epigenetic templates, which implies that structural information as a

subspecies of mechanistic information is carried by these as well. Still, it is DNA

sequences that are originally sequence-specifying, whereas RNA sequences and

epigenetic state-modifications are only derivatively so. Furthermore, other factors

that take part in protein synthesis are at most sequence-modifying, i.e., they do not

act as templates themselves but only modify pre-existing templates. They are

therefore not sources of a structural information flow.

However, despite the primacy of genes in the structuring of amino acid chains of

proteins or polypeptides, genes do not have any primacy with regard to their

regulatory role. DNA sequences are on a par with other factors, including RNAs and

epigenetic ones, in so far as regulation is concerned, and the highest level of

regulation belongs to the system itself, i.e., living systems are self-regulating from

the cellular level onwards. Developmentalists are therefore right in their rejection of

any claim that genes possess regulatory primacy in the form of controlling power

over living systems. One way of establishing this, which is less radical than the

approach found in developmental systems theory, is simply to point out that protein

synthesis also takes place independently of development in the strict sense, which

entails a succession of developmental stages. We may stick to the metabolic or

adaptive activities of an organism at a specific stage of development, as does Bogen

and Machamer (2011), in which case there is no developmental role in the strict

sense for genes to play. The genes in question may just be ‘housekeeping’ ones.

What drives the protein synthesis involved in housekeeping is not the genes, though

the latter play a unique role in it by virtue of their structuring power. Rather, protein

synthesis is part of a self-regulating system where there are very general system

needs for certain proteins to be synthesized and therefore templated, at least

partially, by the appropriate genes. Additionally, there are more specific system

needs for certain proteins to be synthesized, for instance, in response to external

stimulation.

If we do bring in development in the strict sense, we may still conceive of

systemic goals or needs that are to be fulfilled at various developmental stages.

Thus, selector genes template transcription factors that take part in cell differen-

tiation and thereby contribute to the body plan of the organism. Development itself

is not controlled by these genes, though, but by the system of interacting

components. Such a system is of course not only self-regulating but even self-

structuring. Still, there is a privileged level of sequence-structuring at work by way

of structural mechanistic information.

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123

Such mechanistic information contrasts sharply with semantic information. Since

genes do not have any controlling power, they fall short of being instructions that

are carried out by the rest of the cellular machinery. Recently, both Stegmann and

Nicholas Shea have argued that genes do indeed have instructional content (Cf.

Stegmann 2005; Shea 2007). While Shea’s argument is based on the evolutionary

role of genes and Ruth Millikan’s teleosemantics, Stegmann’s criterion for

instructional content is a minimalist one based on their developmental role. Thus,

unlike Shea, Stegmann does not require that there is any natural selection for the

causal correlations involved, or that there is a reader or consumer of the information

in question. He has argued that both the replication code and the genetic code in

prokaryotes show that genes have ‘‘instructional content’’ in these cases, and

therefore semantic content of sorts. If this were indeed the case, structuring and

regulatory power would be brought together in genes, as it were, and they would

control the very processes of DNA replication and protein synthesis. Stegmann’s

argument is by way of an analogy with computer programs or cake recipes, with

instructions arranged sequentially, just as DNA or RNA bases or base triplets. There

is also the possibility of error in the execution of the instructions because of the

codes involved, i.e., even if x codes for y it may not produce anything at all or it

may produce z = y.

Against this, it may be objected that sequential arrangements are characteristic of

the encoding and encoded code-script of a structuring code as such, and do not

indicate that we are dealing with instructions. In the replication and transcription

codes, the encoding modular units are freely permutable in such a way that if they

were to be instructions we would still have a well-behaved execution of these,

whereas this is not generally the case with instructions of computer programs or

cake recipes. This is consistent with the idea of coding regions of DNA constituting

mere data to be read in a cellular program, by polymerase enzymes and ribosomes.18

Indeed, we do not need to speak of a program at all, and thus neither of instructions

to be executed nor of data to be read and written, since it is not necessary to bring in

semantic information. It suffices to acknowledge genes as carriers of structural, or

sequence-specifying, mechanistic information in a self-regulating system. The

notion of templating resources that carry ‘‘stored’’ structural information, and which

are ‘‘called upon’’ by the living system to fulfil a system goal, might then replace the

developmental notion of information in the form of instructions that are executed in

Stegmann (2005), as well as the more recent proposal of genetic ‘‘sequence control’’

in Stegmann (2012a). Genes would not possess any controlling power that would

amount to regulatory primacy in terms of their fulfilment of system needs, since the

overall control belongs to the living system itself.

Shea’s suggestion, on the other hand, relies on bringing in the evolutionary rather

than developmental role of genes, and therefore on a historical property of genes. If

there is a mutation for thick hair in a mammal, and there has been natural selection

for this mutation, the gene in question has both a descriptive and a prescriptive

semantic content. The former is ‘it is cold’ and the latter is ‘grow thick hair’.

18 In Woese (1967) it is suggested that DNA and RNA make up two classes of informational molecules,

corresponding to «tape» and «tape readers», respectively. This is a modification of that proposal.

F. Kjosavik

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Whereas there is only the possibility of error in Stegmann, there would seem to be

the possibility in Shea of both misrepresentation and misinterpretation. The former

is the case when it is not cold and the gene is still expressed in the mammal. The

latter is the case when thick hair is not grown, even if the gene is to be expressed in

the mammal. Shea in effect adopts a semantic stance towards causal correlations

between environmental conditions, like temperature, and genes, as well as between

genes and the phenotypic differences they make, like growth of thick hair, in so far

as these correlations are established through natural selection.

However, a categorical difference between genes and non-genes is manifest even

on the first occurrence of a gene in a line of descent, and this difference therefore

cannot lie in the historical property of having been selected for. It consists, rather, in

the fact that even this occurrence has structuring power and carries mechanistic

information. Furthermore, according to Shea, semantic, as opposed to mechanistic,

information can be carried only by zygotic DNA in multicellular organisms,

whereas DNA downstream of this in cellular development is assigned a mere

developmental and therefore non-semantic role. Again, this does not seem to do

justice to the categorically different way of difference-making that is manifested by

genes in metabolic activities and throughout developmental stages of a life cycle.

The primacy of genes when it comes to sequence-structuring is not merely a

matter of molecular details, then. Rather, as noted repeatedly above, it is very

important in an account for the high fidelity, or robustness, of genetic transmission

across cell generations and the high level of stability, or robustness, in protein

synthesis from which other stable processes, including cell reproduction, benefit.

The very relation between the primary structure of a protein and its higher order

structure through molecular folding is a source of qualitative novelty in the form of

emergence of highly diverse protein functions. The mapping of mutations in the

genetic code-script onto chains of amino acid residues by way of transmission of

structural information is therefore the basis of inheritance of variations of a very

wide scope, and thereby for much of the diversity on which natural selection acts.

This brings out the evolutionary importance, then, of primacy in the sequence-

structuring role and power of genes, in the form of original sequence-specification,

even if there is restricted parity between genes and non-genetic factors—in a no-

dichotomy sense as well as in a distributive sense, i.e., parity in specification of

traits in general as well as in regulation of life processes.

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