Rautian, 1993. On the nature of the genotype and heredity

UDC 575. 1/16 On the Nature of the Genotype and Inheritance A. S. Rautian The dual nature of the genotype is examined as both a material carrier and simultaneously the content of hereditary information from the perspective of A. A. Lyapunov’s principle of the relativity of information content. A view on the nature of inheritance is presented, continuing the development of the epigenetic theory of evolution initiated by M. A. Shishkin in the development of the theory of stabilizing (canalizing) selection of I. I. Schmalhausen and C. H. Woodgington. The term “genotype” denotes simultaneously hereditary information and its material carrier (Schrödinger, 1947). Since the genotype as a carrier of hereditary information is chemically specific, it is sometimes referred to as the “substance of heredity” (Kellaway, 1986). Before the era of information theory this did not cause bewilderment, although the founders of Morganism already wrote in 1915: “The assumption that chromatin particles, indistinguishable from one another and almost homogeneous under any known methods of investigation, can by virtue of their material nature endow all the properties of life exceeds the imagination even of the most convinced materialist” (Morgan, Sterevant, Miller, Bridges – cited in: Kellaway, 1986, p. 35). In our time these concerns have been confirmed. Information is an expression of the diversity reflected by the subject, contained in the structure of the object with which the subject interacts (Ashby, 1959; Berg, Spirkin, 1973; A. S. Rautian, 1988) and in this sense does not constitute an independent entity (Seravin, 1973; Wiener, 1983; Korogodin et al., 1991). A fundamental property of information turned out to be the relativity of its content: a very weak connection of the latter with the properties of the material carrier (the genotype in the second sense), in particular with the way information is coded and the number of signs used for this, and a very strong dependence of the content on the properties of the information receiver, primarily on the level of its prior inform­ation (Lyapunov, 1980) – competence (Woodgington, 1964; Belousov, 1980, 1987). “The same object can be a carrier of one piece of information or another. Depending on which system receives the same signal, it may have one meaning or a completely different one” (Lyapunov, 1980, p. 321). At the same time information is material in the sense that it “always needs a material carrier. Outside matter information does not exist, yet carriers of the same content can be completely different objects… Both the physical carrier and the way information is coded on a given carrier can be entirely different, while the content of the information portion remains the same. There is no link between the mass and energy of the information carrier and its content, and the link between the properties of the carrier and the number of signs recorded in it is very weak. It is largely determined by the chosen coding method” (Lyapunov, 1980, p. 322). Hereditary information (genotype in the first sense) is addressed to the ontogenetic system – the phenotype (Spearman, 1925; Morgan, 1937; Woodgington, 1947, 1964, 1970; Child, 1948; Timofeyev‑Resovsky et al., 1966; Svetlov, 1978; Watson, 1978; Belousov, 1980, 1987; Stent, Keldingar, 1981; Hessin, 1984; Shishkin, 1988a,b). Consequently (see briefly: Rautian, 1991): 1. The content of the genotype is not so much a consequence of its properties as a material carrier of hereditary information as a consequence of the properties of the phenotype to which it is addressed. Therefore, at different stages of ontogeny and during different morphogenetic processes the phenotype extracts from a fundamentally identical genotype (only replicated, multiplied by the principle of equal‑inheritance cell division: Wilson, 1936; Hartmann, 1936) information of varying content (Drish, 1915; Spearman, 1925; Woodgington, 1947, 1964, 1970; Child, 1948; Svetlov, 1978; Belousov, 1980, 1987). It is not accidental that the fundamentally pre‑formational theory of embryonic plasma of A. Weismann (1918) assumed unequal inheritance, and chromosomes were not regarded there as direct carriers of heredity. Thus, the phenotype is the embodiment of an active functional principle in the organism, and the genotype is the embodiment of a passive structural principle (Schmalhausen, 1968, 1969, 1982, 1983). This should also be the relation between the ideal user and the information keeper: any movement (in particular, functioning) reduces the stability of the carrier and therefore the reliability of information storage (Ashby, 1959, 1962; Brillouin, 1960, 1966; Shannon, 1963; Beer, 1963; von Neumann, Morgenstern, 1970; Wiener, 1983). It is no coincidence that the lion’s share of mutations arises at moments when DNA molecules are involved in functional processes, i.e., during their replication in cell division and protein synthesis (Watson, 1978; Stent, Keldingar, 1981; Hessin, 1984). 2. The definiteness of genotype content depends less on the stability of its elements – genes – than on the stability (definiteness of properties) of the historically formed, i.e., pre‑informed, phenotype of the adaptive norm at all ontogenetic stages (Schmalhausen, 1940, 1968, 1969, 1982, 1983; Shishkin, 1981, 1984a,b,c, 1987, 1988a,b). The adaptive norm (“wild type”, standard phenotype) can be defined as the set of life cycles of individuals of a given species or their stages, arising as a historically (phylogenetically) justified stable (hereditary and adaptive) response to the influences of a historically typical internal and external environment (Kostina et al., 1982; A. S. Rautian, 1988). In the case of high integrity, stability and discreteness of different adaptive reactions of organisms (polymorphism according to: Berg, 1957) one can speak of several norms within the overall adaptive norm of the species (Schmalhausen, 1968). The greater stability of the adaptive‑norm phenotype compared with its genotypes, predicted by I. I. Schmalhausen (1938) and following, in particular, from the fact of population saturation with diverse hereditary changes (genovariations) under the guise of a uniform stable “wild‑type” phenotype (Chetverikov, 1983; Ayala, 1984) – the adaptive norm – receives increasing experimental confirmation (Koen, Shapiro, 1982; Hessin, 1984). In this, and only in this sense, the statement that the norm of response, rather than organismal properties per se, is inherited is justified (Woltereck, 1909; Rieger, Michaelis, 1967, p. 360). Inheritance of a trait does not occur as transmission of a more or less pre‑formed germ, as A. Weismann (1918) supposed; only a sufficiently general developmental plan and its control are inherited (Shishkin, 1981, 1984a,b,c, 1987, 1988a,b). The latter is realized by periodic (during critical periods of development, see Svetlov, 1960) increase of the sensitivity of a given morphogenesis to the overall ontogenetic state and to external environmental factors (Dorfman, Severtsov, 1984; Shishkin, 1988a,b). Continuous control is impossible because it would be equivalent to permanent sensitivity and therefore instability (A. S. Rautian, 1988) of morphogenesis. Hence, between critical periods the morphogenetic apparatus (Filatov, 1939) develops substantially autonomously and mosaically relative to others (Schmalhausen, 1982; Shishkin, 1988a,b). Thus, trait formation in ontogeny, carried out overall as epigenesis, for most of the time proceeds in a manner approximating pre‑formation. This underscores the organizing role of short critical periods of development (reorganization of morphogenetic fields, see Gurvich, 1944), taking into account the inertia of their consequences (developmental settings, see Ivanov, 1937) under conditions of strong continuity across successive ontogenetic stages (A. S. Rautian, 1988). Control of the overall course of ontogeny is carried out by periodic and largely asynchronous alignment of individual morphogeneses with the state of the developing organism as a whole (Gurvich, 1944; Woodgington, 1947, 1964, 1970; Svetlov, 1978; Belousov, 1980, 1987; Shishkin, 1988a,b). Synchronization of critical periods of many individual morphogeneses during catastrophic metamorphosis (Tokin, 1987) is possible only thanks to its historical (phylogenetic) preparation (Shishkin, 1981, 1984a,b,c, 1987, 1988). However, complete synchronization in the general case would imply a sharp disruption of continuity between ontogenetic stages separated by metamorphosis, which, given the sensitivity of morphogeneses in the critical period and the long‑lasting inertia of its consequences, would lead to a chain reaction of degradation, destroying the already formed organization at subsequent developmental stages (A. S. Rautian, 1988). Metamorphosis is characterized by regulated and reversible degeneration, reversible in the sense that after the inevitable partial (especially strong in necrobiosis‑type metamorphosis, accompanied by lysis of larval structures and a pause in animal motor activity, see Tokin, 1987) degeneration during catastrophic metamorphosis, processes of progressive differentiation, integration and growth of the organism’s organizational level are restored. Thus, the asynchrony of critical periods of individual morphogeneses creates an overall impression—generally a false one—of graduality and uniformity (gradualism, per Godri, 1896), constant directionality and relative non‑conflict (in other words, pre‑formation, see Rautian, 1988) of ontogeny as a whole, excluding only relatively brief and, in the general case, non‑obligatory periods of catastrophic metamorphosis. Therefore, unevenness and stage‑wise development are usually easier to establish for a particular morphogenesis than for ontogeny as a whole. Indirectly, empirical principles of equifinality (Drish, 1915; Gurvich, 1944; Svetlov, 1978; Belousov, 1980, 1987; Shishkin, 1981, 1984a,b,c, 1987, 1988) and equal‑inheritance division support epigenesis. The phenomenon of equifinality is expressed in the ability of the adaptive‑norm ontogeny, as it proceeds, to correct not too large (but also not arbitrarily small) deviations in the initially largely genotypic developmental conditions that arise during their realization. Equifinality results from the increasing overall effectiveness (“power”) of the regulator (Rasnitsyn, 1966) as the level of organization of the self‑organizing organismal system grows (Beklemishev, 1970; A. S. Rautian, 1988). “With development the organism’s autonomy relative to its environment increases… as does the definiteness of its form” (Bär, 1950, p. 369). The growth of regulator “power” is caused by an increase in the potential (though not necessarily realized) sensitivity and precision of reception of internal and external environmental parameters (Volkenstein, 1988), as well as by an increase in the diversity and accuracy of the organism’s responses to perturbing influences as the level of organization rises (A. S. Rautian, 1988). It may seem that the notion of equifinality conflicts with K. E. von Bär’s (1950) law of the order of ontogenetic differentiations: “1) … in each large group the general form arises before the special… 2) In the relations between forms, from the general a less general one arises, and so on, until finally the most special appears” (pp. 320‑321). However, the lion’s share of the empirical material underlying the law, as can be seen even from Bär’s wording, concerns organisms of different supra‑specific affiliations, whose ontogenies, at least from the moment of their deviation, by definition lack common equifinal states. Individual differences, fully consistent with Bär’s law, arise only at the very latest and most mosaically realized developmental stages (since the formation of developmental settings precedes their implementation; see Schmalhausen, 1982), for which the property of equifinality manifests only within each individual autonomously operating morphogenesis. Indirectly, the relatively high phylogenetic lability of the final ontogenetic stages compared with early ones (Haeckel, 1939; Severtsov, 1939; Shishkin, 1981, 1984a,b, 1987, 1988a,b) testifies to the correctness of the latter proposal, reflecting Bär’s law in empirical form. This lability, in turn, is caused by the terminal and mosaic nature of the corresponding stages, which hinders the amplification of emerging deviations during the brief subsequent development (Schmalhausen, 1968, 1969, 1982, 1983). The picture of development described above aligns well with the notion of an ideal complex purposeful process, namely ontogeny. Periodic correction of the trajectory of such a process proves to be a significantly more effective means of its regulation than attempting a rigid algorithmic specification of the entire trajectory at the level of initial conditions. Algorithmic specification of the whole ontogenetic trajectory at the level of initial conditions fits well with the notion of pre‑formation, which found its most consistent expression in A. Weismann’s theory of embryonic plasma (Shishkin, 1981, 1984a,b,c, 1987, 1988a,b). In the case of periodic correction, the noise‑immunity of ontogeny can be much higher, and the specific cost of its energetic and informational support much lower, than in the former case (Beer, 1963; von Neumann, Morgenstern, 1970; von Neumann, 1961; Wiener, 1983). Equal‑inheritance division makes this more efficient mode of ontogenetic regulation possible, because at the level of initial conditions (in the zygote) it is not precisely specified which future embryonic cells will require which particular hereditary information (e.g., Belousov et al., 1974, 1976). As noted above, A. Weismann was not accidentally a proponent of unequal inheritance, since it better accords with his doctrine of inheritance of pre‑formed germinal elements, equivalent to assigning hereditary traits of ontogeny at the level of its initial conditions. The regulatory mechanism that maintains ontogenetic stability by periodic correction of its trajectory resolves the contradiction of the greater stability of the functioning phenotype compared with the passive genotype protected from metabolism. The regulatory mechanism that maintains phenotype stability, inconceivable outside metabolic activity, surpasses in efficiency the passive mechanism of setting the genotype at the level of ontogenetic initial conditions (in the zygote). Protection of the genotype from the metabolic activity of the organism’s phenotype limits the possible effectiveness of repair processes, which, however, also have a functional, i.e., phenotypic, nature. Thus the question arises: would it not be better to replace the structural rigidity of the genotype with a regulatory means of maintaining its stability? Indeed, a partially regulatory mechanism is already used in the form of repair. But a complete replacement of this kind is impossible. In fact, any purposeful functioning is possible thanks to a more or less rigid structure that channels function by limiting the diversity of its manifestations (Ashby, 1959, 1962; Brillouin, 1960, 1966; Shannon, 1963; Beer, 1963; Wiener, 1983; A. S. Rautian, 1988). The genes of the genotype themselves constitute a system of such control limiters. At the same time, it must be remembered that the role of limiters (switches) as such can be nonspecific, similar to river banks, which are not the cause of water flow, or a telephone exchange composed of continuous switches that themselves do not produce or transmit, but only direct signals. Moreover, incorporating these limiters (switches, directors) into movement processes immediately reduces their noise‑immunity and thus the reliability of operation. A stationary regime with lower noise‑immunity of rigid structures can be maintained only under conditions of their reproduction in functional processes. The mechanism of such reproduction is the replication of the genotype in cell and organismal reproduction. 3. The genotype possesses a well‑defined content only for an already (to a known degree independently) inherited phenotype from the mother or a preceding ontogenetic stage. In ontogeny the “role of reproduction is that part becomes whole” (Bär, 1950, p. 369). This is evidenced, in particular, by the absence of translation of genetic information at cleavage stages in many organisms, which in some organisms is delayed until gastrulation and even neurulation, when the basic plan of the organism’s structure is laid down (Belousov, 1980, 1987; Shishkin, 1988a,b). In other words, in ontogeny a competent consumer of hereditary information is first created (Woodgington, 1947, 1964, 1970; Belousov, 1980) and only after that its use begins, not merely its replication during cleavage. Consequently, any reproduction bears the traits of vegetative reproduction, or uses another’s phenotype as a source (viruses). The latter case, of course, is possible only as a result of historical (phylogenetic) acquisition by the parasite of certain specific functions of the host’s phenotype. An organizational prerequisite of such adaptation is the high invariance of the genetic code of all living beings and the high semantic universality of some of its units. 4. The genotype as the entirety of an organism’s hereditary information (Johansen, 1933, 1935; Rieger, Michaelis, 1967, pp. 82, 152; Ayala, 1984) cannot be localized in primary nucleic‑acid structures (which follows from point 3); it is an aspect of the phenotype, not a part of it, and in this sense does not constitute an independent entity (Baur, 1913; Lyubyshev, 1925; Goldschmidt, 1940). On this matter, already at the dawn of genetics K. A. Timiryazev wrote: “A considerable confusion of concepts, as Arthur Thomson rightly noted, is introduced by borrowing from jurists the notions of inheritance and heirs for the theory of heredity.”They speak of a transition to the organism of a particular inheritance, while in nature the heir and the inheritance are the same object—the inheritance is the heirs themselves and their parts» (1939a, p. 166). “Each trait of organization is hereditary, consequently every random change is hereditary. Heredity is a necessary phenomenon” (1939b, p. 119). Indeed, a strictly non‑hereditary change presupposes its occurrence contrary to the hereditary constitution of the organism. Yet if such a change arises, the organism must have had a precondition for its emergence. No external influence can produce what is prohibited by the organism’s constitution. Any change in the organism has its precondition in its heredity. As C. Darwin wrote (1939, p. 278): “…a non‑hereditary change is not essential for us.” The precondition for the emergence of a strictly non‑hereditary character cannot arise in the course of phylogenesis, which contradicts the notion of the historical formation of organismal constitutions. The term “non‑hereditary character” (more precisely, low heritability) is used when the stability of the ontogenetic trajectory (creoda, see Waddington, 1964, 1970) leading to its phenotypic realization is relatively small (Shishkin, 1981, 1984a,b, 1987, 1988a,b). To a greater or lesser extent, this property is possessed by all deviations (aberrations, according to Semenov‑Tyan‑Shansky, 1910) from the adaptive norm—the “wild type” (Schmalhausen, 1968, 1969, 1982, 1983; Shishkin, 1981, 1984a,b, 1987, 1988a,b; Goldschmidt, 1938, 1940, 1955; Waddington, 1953–1966). It is not accidental that A.P. Semenov‑Tyan‑Shansky regarded the absence of inheritance of aberrations by the direct offspring of their bearers in natural conditions as a rule. All these inferences are consistent with the empirical rule of heredity formulated by C. Darwin (1939, pp. 278‑279): “The number and variety of hereditary deviations in structure, both trivial and very important physiologically, are infinite… Every breeder knows how strong the tendency toward hereditary transmission is; that ‘like produces like’ is his basic conviction; doubts about this have been expressed only by theoreticians… Perhaps the most correct view on this subject would be to consider the inheritance of each trait a rule, and its non‑inheritance an exception.” The genotype, as the material carrier of all hereditary information, is identical with the phenotype because: a) in the absence of a competent recipient (reader) it is meaningless to speak of a specific content of information (Lyapunov, 1980); b) continuity (including between generations) ultimately ensures the entire structure of the organism (A.S. Rautian, 1988). The opposition of the concepts “genotype” and “phenotype” is more operational, i.e., epistemological, than ontological. 5. Each element of the phenotype, including the genotype, is both a recipient and a carrier of hereditary information relative to other phenotype elements. This is evidenced by ontogenetic correlations (Schmalhausen, 1939, 1968, 1969, 1982, 1983), inductive interactions among parts of the developing embryo (Shpeman, 1925; Waddington, 1947, 1964, 1970; Svetlov, 1978; Belousov, 1980, 1987), often linked by feedback relations (Zavadovsky, 1981), and by the long‑term existence (especially at middle and late ontogenetic stages) of autonomous and mosaic morphogenetic apparatuses, in which the same parts alternately act as inducer and as reaction system. In this case, inducing influences are usually nonspecific (signalling) in nature, merely revealing the competence of the reaction system (Balinsky, 1936; Filatov, 1939; Svetlov, 1978; Belousov, 1980; Schmalhausen, 1982). If we now mentally transfer the notion of a nonspecific (sign‑like, syntactic: Kondakov, 1975, p. 543) impact that reveals competence (semantic specificity: Kondakov, 1975, p. 526) of a reactant to “chromatin particles,” we obtain a solution to the problem formulated by the founders of morphogenetics already in 1915: how can “chromatin particles…, by virtue of their material nature, endow all the properties of life”? (see the introductory section of the article). “Chromatin particles” per se lack the specific properties of the living, foremost active functioning and, consequently, an effective regulatory mechanism for maintaining their stability. Hence, belief in their ability to “endow all the properties of life” truly “exceeds the imagination of the most convinced materialist.” Nevertheless, it is quite plausible that “chromatin particles,” through nonspecific impact on a competent (by virtue of prior phylogenetic history) and “all‑life‑properties” endowed phenotype, can reveal (detect) the “properties of life” inherent to the latter. Since the genotype as a carrier of hereditary information represents not a functional but a “structural basis of heredity” (Morgan, 1924), the capacity of chromatin particles for such nonspecific (signalling) impact is transferred to the functioning phenotype, which in turn, to the extent of its competence, reveals the biologically significant role of chromatin, as well as of its other components—such as water, salts, carbohydrates, lipids, proteins, etc. In this sense, the phenotype constitutes the sole yet holistic (i.e., divisible only for operational purposes) functional basis of heredity. 6. The genotype as the genetic code is a specialized, but far from the only, “organ” for storing and transmitting hereditary information of any content. Restrictions apply only to the form in which the content is embodied, which is accessible only to a competent user—that is, to the material carrier’s form. For example, the chemical specificity of the genetic code protects it from involvement in the myriad metabolic processes occurring in the cell. 7. “We have every reason to assert that in nature there are no two absolutely identical genotypes” (Paramonov, 1967, p. 10). The strict requirement of isomorphism of genotypes both in composition and in allele order on chromosomes is usually argued with examples of huge phenotypic consequences of single macro‑mutations on the one hand, and the near‑absence of such consequences for numerous small mutations on the other (Timofeev‑Resovsky, Ivanov, 1966; Timofeev‑Resovsky et al., 1969). While logical, this approach inevitably leads to the conclusion of strict non‑inheritance of genotypes, at least in eukaryotes. Indeed, the spontaneous mutation rate per locus is on the order of 10⁻³–10⁻⁶, and the number of loci in a eukaryotic genome is on the order of 10⁴–10⁶ (Dubinin, 1966; 1976; Luchnik, 1978; Levonti, 1978; Gershenson, 1983; Ayala, 1984). From this it follows that a single spontaneous mutational event, without accounting for other recombination forms (which occur far more frequently), is sufficient to make the probability of even a single exact genotype repeat low, even over a long history of a highly fecund species. If one recalls that the norm of reaction, by definition, is determined by the genotype, then the classic genetics generalization that “it is not the property per se that is inherited, but only the organism’s norm of reaction” (Rieger, Michaelis, 1967, p. 360) turns out to be false. Genes are inherited, but not genotypes; adaptive norms, but not reaction norms. The non‑inheritance of the genotype and of the reaction norm brings them closer to the usual notion of a phenotypic trait that is not inherited as such. This aligns well with the proposal of item 4. Moreover, the non‑inheritance of the reaction norm excludes it from operational, i.e., experimentally respectable, concepts. Indeed, if each individual has a unique genotype and thus a unique reaction norm, experimentally only one realization of it can be obtained. The reaction norm as a spectrum of phenotypic responses possible on the basis of a given genotype lies beyond the reach of experimental methods. Hence it is difficult to agree with the following characterization (Schmalhausen, 1968, p. 25): “The concept of ‘norm of reaction’… is one of the few strictly defined notions that allow full clarity in the debated questions about forms of variability and their significance in evolution… Mutation means a change… in the organism’s reaction norm…”. The observed contradiction results from an unjustified extrapolation of genetic analysis of a few traits and loci to the overall structure and relationship of phenotype and genotype. G. Shpeman (1925) wrote already in 1924: “The concept ‘hereditary’ rests on pre‑scientific thinking. From ancestors comes both movable and immovable property, and from one to another completely defined things are transferred. One individual receives from another something that enriches him, but without which he could manage. Genetics selects a single property and opposes it to the whole set of other properties, which constitute the constitution of the individual. For each single trait one can say that the child inherited it from its ancestors, but this cannot be said of the whole set of traits, for that would imply that the child inherited the beginnings of itself” (cited in: Korotkova, Tokin, 1977, p. 3). It is instructive to note the common starting premises of Shpeman and Timiryazev (see item 4), as well as the fact that the idea of “inheriting the beginnings of oneself” from ancestors was not foreign to A. Weissman (cf. items 1 and 2). This overly bold, yet at the turn of the century psychologically understandable extrapolation has become in our time an obvious, though not yet eradicated, anachronism. 8. “Genotype is the genetic organization of an individual at one or several considered loci” (Ayala, 1984, p. 204). This strictly operational (not ontological) definition of genotype is the only experimentally respectable one, yet it is also the least frequently used. Even in the cited book by F.D. Ayala it is only the second of two definitions of the term (the first being quite traditional). In this sense the genotype is unquestionably inherited, but its reaction norm can be studied only if all other (experimentally unconsidered) organismal properties are sufficiently invariant. The entire genotype of an organism, as follows from item 7, cannot be such an invariant. Only the genotype in the operational sense can serve this role, but in any real experiment it covers only a negligible part of the individual’s genetic organization. In practice, the “wild type” or an artificially stabilized breed or variety phenotype—i.e., the adaptive norm—is used as the invariant in all reaction‑norm phenogenetic experiments; its invariance, as already mentioned (item 2), is achieved not by uniformity of the underlying genotypes but despite their diversity. Thus, all experimental data on reaction norms are collected not against an invariant genotype but against a stable adaptive norm, which, unlike the genotype (in the broad sense), evidently is inherited. In other words, the traditional interpretation of experimental data on adaptive norms presents the desired as the actual. 9. A sufficiently rigid association of individual genetic code symbols (genes) with phenotypic traits expresses the stability of the reaction system corresponding to the adaptive norm (Schmalhausen, 1940, 1968; A.S. Rautian, 1988), against which we observe isolated (elementary) disturbances (Rautian, Rautian, 1985), rather than a similarly rigid causal dependence of traits on specific genes. This is demonstrated by experiments in which the gene‑trait link is radically altered (Waddington, 1953, 1957, 1966; Kamshilov, 1972), and by comparative‑morphological studies reconstructing the probable phylogeny of such changes (Rautian et al., 1985; Rautian, Kostina, 1985; G.S. Rautian, 1988). The very possibility of such phylogenetic reconstructions indirectly indicates that irreversible population transformations (Schwartz, 1980) in the gene‑trait relationship mark elementary micro‑evolutionary changes that already have phylogenetic significance (G.S. Rautian, 1988). The absence of a strict causal dependence of traits on specific genes is also indicated, as mentioned in item 8, by the fact that the stability of the adaptive norm is ensured not by uniformity of its genotypes but despite their diversity (Schmalhausen, 1968, 1969, 1982, 1983; Shishkin, 1981, 1984a,b,c, 1987, 1988a,b). The notion of high genotypic diversity in a population, veiled by a uniform adaptive‑norm phenotype, fits well with Bridges’ balance model of population genetic structure (Bridges, 1922; Ayala, 1984). Moreover, the impression of a strict causal link between traits and particular genes stems from the logical inconsistency of the usual method of interpreting genetic experiments. From the validity of a direct statement in the general case, as is known, does not follow the validity of the converse (Aristotle, 1978): if a stable association exists between a “mutant” trait and a well‑defined mutant allele (the stability of which is usually exaggerated) (Schmalhausen, 1968, 1969, 1982, 1983; Shishkin, 1981, 1984a,b, 1987, 1988; Babkov, 1985), it does not follow that the “normal” allele of the same gene is equally responsible for the normal trait of the same species (Goldschmidt, 1938, 1940, 1955). Indeed, on genetic maps loci are marked by “mutant” traits (Zakharev, 1979). This is not accidental, because no one knows exactly which “wild‑type” (adaptive‑norm) trait a “normal” allele governs. No one dares to treat visible traits the same way as alleles (to assume that a “normal” allele encodes the logical alternative to a “mutant” trait in the “wild type”). Moreover, try to formulate this logical alternative when there is more than one mutant allele. A similar dilemma was already encountered by the theory of presence‑absence (Penny, 1930). The asymmetry of direct and inverse statements in this case necessarily follows from the asymmetry of causal conditioning of normal and “mutant” traits. In the first case, the cause is the historically (phylogenetically) formed system of ontogeny of the adaptive norm of the species. This teleological cause (causa finalis, see Aristotle, 1981) is fundamentally complex both phylogenetically and ontogenetically and cannot be reduced to the functions of one or a few genes (the genotype in the operational sense). Even if a trait is not an obligatory attribute of the adaptive norm and appears only as an adaptive modification under certain internal (e.g., sex‑chromosome balance) and/or external conditions, the latter act as efficient causes (causa efficiens, see Aristotle, 1981) that merely release the morphogenetic process leading to the formation of the trait, but are not the cause of the process itself, nor of the trait (Schmalhausen, 1968, 1969, 1982, 1983; Shishkin, 1981, 1984a,b,c, 1987, 1988a,b). In phylogenesis, the emergence and phenotypic expression—specificity (Timofeev‑Resovsky, Ivanov, 1966)—of a trait are mutually conditioned. Therefore, separating their teleological causes is meaningless. Conversely, a “mutant” trait as such arises not because of, but in opposition to, the preceding history of the species. The cause of the trait’s emergence (expression) in this case is naturally taken to be the operative cause of homeostatic disruption—a historically atypical internal (e.g., a “fresh” mutation: Schmalhausen, 1968) and/or external agent for which the organism lacks a historically prepared response base—competence (Schmalhausen, 1968, 1983; Shishkin, 1987, 1988). An agent of this kind usually induces indeterminate variability (Darwin, 1939, 1951; Schmalhausen, 1968, 1969, 1982, 1983; Shishkin, 1981, 1984a,b, 1987, 1988a,b), which indicates: a) semantic indeterminacy of the signal generated by this agent for its recipient—a reaction system incompetent with respect to it; and b) the existence of a broad logical space of variability (Zavartsin, 1974) veiled in historically typical developmental conditions by a stable adaptive‑norm phenotype and partially revealed under the influence of the historically atypical agent’s signal. Thus, indeterminate variability indirectly supports the view of a strong dependence of information (signal) content on the properties (competence) of its recipient, as A.A. Lyapunov wrote (see the article’s beginning). The complex nature of the consequences of a historically atypical operative cause is no less probable than the more pronounced homeostatic function of the organism: the ontogeny of its offspring across generations. Here the notion of an elementary cause of disruption, which may be a point mutation, is quite appropriate. Indeed, deviations from the adaptive norm (aberrations) cannot be interpreted as adaptive polymorphism arising under the action of a special selection vector toward a discrete stable expression of polygenic trait complexes.The evolutionary fate may be reduced solely to the neutralization in the phenotype of the hereditary basis (evolution of recessiveness, etc.; Shmalhausen, 1968, 1982) as a result of stabilizing selection acting on variants of the adaptive norm and to be expressed in the emergence of stability (discreteness) of the latter with respect to deviations from it (Shmalhausen, 1940, 1968, 1969, 1982, 1983). Consequently, the reliability of judgments concerning the simplicity of provision (by one or a few tightly interrelated genes or morphogenetic factors in their manifestation) for recurrent aberrations is considerably higher than for phenotypes of the adaptive norm (Rautian, Rautian, 1985; Rautian, 1990). Historically atypical operative causes of the emergence (expression) of a trait do not imply the absence of historical conditioning (teleological cause) of its specificity, which, as we have seen, has a fundamentally complex character. Indeed, the cause of the specificity of deviation (in particular, a “mutant” trait) lies in the construction of the adaptive norm, the violation of which it represents. A more stable phenotypic expression of normal traits compared with “mutant” ones (manifested in the uncertainty of expression and low frequency of the latter) indicates lower stability and purposiveness of deviation morphogenesis compared with those of the adaptive norm (Shmalhausen, 1968, 1969, 1982, 1983; Shishkin, 1981, 1984a,b,v, 1987, 1988a,b; Goldschmidt, 1938, 1940, 1955). Thus, one can confidently speak of the complex nature of teleological causes and the usually elementary nature of operative causes. The former determine the emergence of normal traits and the specificity of expression of normal and “mutant” traits. The latter determine the emergence (expression) but not the specificity of expression of “mutant” traits and may determine the manifestation in the phenotype (but not the emergence) of normal traits. Consequently, a “mutant” trait can be used to mark a locus on a chromosome (for example, when constructing genetic maps), which may carry either a mutant or a “normal” allele. However, from the viewpoint of operative cause, the more or less defined association of a mutant allele with a “mutant” trait and a normal allele with a normal trait is often caused by a causal link of the former, but in general it says nothing about the presence or absence of a causal link of the latter. This is evidenced, in particular, by the fact that loss of a locus (e.g., due to unequal crossing‑over) usually does not disrupt the formation of a normal trait, while in an organism from a mutant line it induces a reversion to the “wild type” (Gershenson, 1983). Causal dependence of a “mutant” trait on a mutant allele in general does not allow one to judge cause versus effect. This is demonstrated by: a) the dependence of pleiotropic gene action on its genotypic (Chetverikov, 1983; Babkov, 1985) and morphogenetic (Astaurev, 1974; Svetlov, 1978; Shmalhausen, 1968, 1969, 1982, 1983) environment; b) the wide distribution of heterogeneous groups (very close phenotypic mutations located in different genome parts) in genetically studied species (Timofeev‑Resovsky, Ivanov, 1966); c) the extensive parallelism of “non‑hereditary” (morphoses, according to Shmalhausen, 1968, 1982) and hereditary (genotype‑conditioned) variability (Goldschmidt, 1938, 1940, 1955; Shishkin, 1981, 1984a,b,v, 1987, 1988a,b). Therefore, geneticists rightly demand confirmation of the genotypic conditioning of a “mutant” trait in genetic analysis (Dubinin, 1966; Babkov, 1985). Consequently, a mutant allele may be sufficient but practically never a necessary condition for the appearance of the given “mutant” trait in the phenotype, i.e., a trait with that specific expression (Goldschmidt, 1938, 1940, 1955; Shishkin, 1981, 1984a,b,v, 1987, 1988a,b). 10. The high semantic universality of certain genetic‑code signs for all living organisms or members of very high‑rank taxa is evidence of deep phylogenetic unity of all extant organisms (Margelelis, 1983; Khesin, 1984), not of an immanent link of these signs as material carriers of hereditary information with the content of the latter (Altschtein, 1987). A.M. Ugolev (1990) showed that an important reason for maintaining such universality by stabilizing selection must be the requirement to preserve the trophic unity of the biosphere as a whole. 11. The biological meaning of structural segregation of the genotype within the phenotype and specialization of the genetic code as a material carrier of hereditary information lies in creating an indestructible pool of hereditary information during ontogeny, necessary for reproduction (repetition of essential traits) and correction of species‑specific ontogeneses over generations (Rautian, 1986, 1988); i.e., phylogenesis according to A.N. Severtsov (1939). Indeed, the basis of any (not only biological) development is a contradiction (Hegel, 1974, 1977) between stability (conservation) and freedom of choice (variability) (Kastler, 1967; Nikolis, Prigogine, 1979, 1990; Ebening, 1979; Haken, 1980; Prigogine, 1985; Prigogine, Stengers, 1986). Complete freedom of choice (realization of the entire logical space of variability, see Zavarzin, 1974) is incompatible with system stability (the subject of development) and therefore with its existence. This is the reason for the selection of systems with more or less stable structure. In this sense, stability is a prototype of adaptation of biological systems. Moreover, the preservation of stable structural parameters ensures continuity across successive states during development (A.S. Rautian, 1988). Stability of an equilibrium system provides rigidity of its structure (Ebening, 1979). Non‑equilibrium dissipative systems ensure stability of structural parameters not so much by rigidity as by constant repair performed by cyclic reversible work of dynamic variables that capture matter and/or energy from the environment and channel their flows within the system to restore structural parameters. The purposiveness of this work, carried out according to the Le‑Chatelier‑Braun principle (Beklemishev, 1970), ensures stable structural parameters through feedback (Belousov, 1980, 1987; Shishkin, 1988a,b; A.S. Rautian, 1988). The work of dynamic variables is a prototype of biological system functioning. Switching to new stable states during development by irreversible restructuring of structure and functions (if any) is accompanied by a reversible decrease in its stability. This inevitably deforms (Hegel, 1974‑1977; Strelchenko, 1980) the structure of the preceding state, equivalent to the loss (irreversible erasure: Lyapunov, 1980) of part of the information about it (A.S. Rautian, 1988). Moreover, the task of structurally providing new functions conflicts with the task of preserving information about already passed states. In other words, fundamentally reversible cyclic processes of functioning (Anokhin, 1978, 1979, 1980), which ensure homeostasis of each given system state, conflict with the requirement of continuity, without which the system’s persistence and trajectory stability (homeorhesis, according to Woodington, 1964, 1970) would be impossible during irreversible state changes (A.S. Rautian, 1988). Both noted circumstances promote the irreversibility of development, do not hinder repeated reproduction of historical experience, and render its accumulation meaningless. Such development reduces to the search for more or less stable stationary (Nikolis, Prigogine, 1979, 1990; Ebening, 1979; Haken, 1980; Prigogine, 1985), if you wish, adaptive states. Yet the possibility of optimizing already existing qualitative adaptations (progressive specialization), particularly functions, is severely limited (A.S. Rautian, 1988). The role of a material information carrier about already passed (and, in ontogeny, not yet occurred) developmental stages can be satisfactorily fulfilled only by a structure possibly more segregated from metabolic (functional) processes in the organism. Solving this problem was the primary cause (causa initialis, see Aristotle, 1981) of segregating the genotype as an “organ” of storage and transmission of information within the phenotype and of specializing the genetic code as a material carrier of hereditary information not only between generations but also between ontogenetic stages. This property of indestructibility during irreversible state changes distinguished hereditary information from all other informational (sign and signal) interactions in the organism. As a result of the irreversibility characteristic of development and the cyclic reproduction characteristic of functioning, it became possible to render these processes non‑alternative by separating (if you like, generating) ontogenetic and phylogenetic processes (A.S. Rautian, 1986, 1988). Irreversible ontogenetic transformations began to be reproduced (albeit only in essential traits, which made their correction possible) across generations, thereby creating a new long‑term type of functioning, not of the organism but of the population‑species, i.e., an evolving system. Development of this new function—evolution of ontogeny (Severtsov, 1939; Shmalhausen, 1968, 1969, 1982, 1983; Shishkin, 1981, 1984a,b,v, 1987, 1988a,b)—has become completely irreversible at any finite time (A.S. Rautian, 1988). Reproduction of adaptive norms of a certain type through repeated ontogeneses across generations gave rise to the phenomenon of the biological species. The possibility of accumulating historical experience and refining it (correction) through repeated use (reproduction) creates the prerequisite for progressive evolution. However, organizational progress (departure from thermodynamic equilibrium with the external environment) increases system vulnerability to internal disturbances and external impacts, as well as its dependence on its own historical experience, whose relative value rises with the overall level of organization. Consequently, organizational progress imposes requirements: a) increased system stability; b) restriction of freedom of choice; and c) increased reliability (indestructibility) of memory (heritability). These contradictions are also resolved by separating ontogenetic and phylogenetic processes. The substrate of phylogenesis—a population with low organizational level (“loose” structure), integrity, continuity of its structure during state changes, and high reversibility of its dynamics—has wide possibilities for choice and indefinitely long development. Ontogeny, thanks to high stability, integrity, and purposiveness of organismal development, quickly creates a high level of organization, whose formation is prepared by preceding ontogenetic evolution (Shishkin, 1981, 1984a,b,v, 1987, 1988a,b). Yet this high level of organization, inconceivable without high stability and sharply limited freedom of choice, combined with high ontogenetic irreversibility (within a single cycle) and lack of further historical perspective, halts further ontogenetic differentiations (Shmalhausen, 1984). Thus phylogenesis proceeds in populations, and its results, due to the perfection of hereditary memory, are fixed mainly at the organismal level and reproduced in a series of repeated ontogeneses (Shishkin, 1981, 1984a,b,v, 1987, 1988a,b; A.S. Rautian, 1986, 1988). Key moments in the formation of a typical ontogeny of multicellular organisms primarily reflect the increasing reliability of storing, transmitting, and using (reproducing) historical experience—the content of hereditary information—as the level of organization rises. The greatest danger in this regard is foreign hereditary information (Beklemishev, 1970), which destroys the mutual coherence of an organism’s historical inheritance. One need only recall the disturbances arising from distant hybridization. This danger is especially great because of the universality of the genetic code and the high semantic universality of some of its signs. In prokaryotes, incorporation of new hereditary information into developmental processes is not strictly limited by specific life‑cycle stages. New hereditary information is highly indeterminate in content: fragments of whole genomes of various sizes can be transferred across substantial taxonomic distances. Different life stages of a single biont may involve different hereditary information (Beklemishev, 1970; Khesin, 1984). In unicellular eukaryotes, incorporation of new conspecific hereditary information is limited to moments of reproduction—maximum differentiation (decrease of stability and increase of freedom of choice). Normally, hereditary information is transmitted via complete genomes. Different ontogenetic stages are carried out (up to spontaneous mutations) on the basis of the same hereditary information. In multicellular eukaryotes, ontogenetic differentiation becomes irreversible, accompanied by programmed death. A new ontogeny begins within the parent organism as a defined part of it (Bär, 1950). Following this logic, transduction of hereditary information in eukaryotes, occurring only with the participation of a prokaryotic biont, is an atavistic pathology (A.S. Rautian, 1986, 1988). 12. All and only living systems possess mutually conditioning processes of individual and historical development. The capacity for such double development was a prerequisite for the storage, accumulation, and use (reproduction) of historical experience and thus for the emergence of biological evolution—the sole specific property of living systems to which all other life‑characteristic properties are linked (Shnol, 1979, 1990). In other words, biological evolution is possible only in the form of ontogenetic evolution (Shishkin, 1981, 1984a,b, 1987, 1988a,b). The very possibility of double development, as we have seen, is structurally conditioned by segregation of the genotype within the phenotype and specialization of the genetic code as a material carrier of hereditary information, i.e., by the separation of structural and functional bases of inheritance. Organisms exhibit double development as ontogeny and phylogeny. Changes of cellular generations in multicellular organisms represent the same processes in a reduced form. Not any arbitrary community of organisms constitutes a living system in the proper sense. This property belongs only to a biocenosis (a formed community, according to Vakhrushev, 1988) capable of repeatedly equifinal (e.g., convergent) reproduction of its characteristic structure by self‑assembly in a historically typical biotope from the species that compose its co‑evolved biota. Self‑assembly is characteristic of all elementary morphogenetic processes, and its relative role is especially great in prokaryotic ontogeny. The self‑assembly process of a biocenosis is analogous to its individual development, which in its highest form acquires the character of endogenous exogenetic succession with a pronounced equifinal effect (Razumovsky, 1981). From this viewpoint, the biota of a biocenosis can be likened to a genotype and reproduced according to organismal development laws, using its inherent hereditary apparatus. Historical development of a biocenosis is its evolution, phylo‑cenogenesis. Thus, the definition above allows, at least for now, to distinguish all known living systems from all non‑living ones. The biosphere, for which individual and historical development are inseparable, by definition (Vernadsky, 1960), is biocosmic, not a living body. 13. 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Vol. 110. pp. 110–172.\nPaleontological Institute of the Russian Academy of Sciences, Moscow\nReceived by the editorial office 25.IX.1992\nON THE NATURE OF THE GENOTYPE AND OF HEREDITY\nA.S. Rautian\nPaleontological Institute, Russian Academy of Sciences, Profsoyuznaia ul. 123, 117868 Moscow\nThe term \"genotype\" is used for both hereditary information and its substantial bearer. The most important property of the information is relativity of its content which means very weak dependence on properties of the information substantial bearer (genotype of the second meaning) and very strong dependence on properties of the information recipient. Hereditary information (genotype in the first meaning) is addressed to the ontogenesis system, that is, to phenotype. From this it follows: 1) The genotype content is determined not so much by properties of its substantial bearer as by properties of the phenotype to which it is addressed; 2) Certainty of the genotype content depends not so much on stability of its elements, genes, as on stability of the phenotype of adaptive norm; 3) Genotype possesses certain content only for a phenotype inherited from the ontogeny of another (maternal) organism or from a previous ontogenetic stage of the same organism; 4) Genotype (and this is true for any hereditary information of an organism) cannot be localized in the primary structures of nucleic acids. It is an aspect of phenotype and not a part thereof and, in this sense, does not possess independent being; 5) Each element of the phenotype, including genotype, relative to its other elements, is both recipient and bearer of hereditary information; 6) Genotype, as genetic code, is specialized but not the only \"organ\" of storing and transferring hereditary information; 7) There are no two identical genotypes existing in nature; 8) The only operational definition of the genotype is its treatment as genetic information localized in one or several loci; 9) A rather strong relation between certain symbols of the genetic code (genes) and certain phenotypic characters reflects stability of the reactional system of adaptive norm; 10) High semantic universality of some symbols of the genetic code indicates deep phylogenetic unity of all existing organisms; 11) The biological sense of structural separateness of the genotype within phenotype is creating and supporting an information pool undestroyable during ontogenetic development; 12) All and only living systems possess reciprocally determining processes of individual and historic development; 13) Heredity, as an ability of descendants to reproduce safely in their ontogeneses the properties of their ancestors, is an integral undecomposable (more precisely, decomposable but for operational purposes) property of life. There is no and could not be any \"heredity substance\", as there is no and could not be an \"information substance\"." }