Current Synthetic and Systems Biology
Open Access
ISSN: 2332-0737
ISSN: 2332-0737
Review Article - (2025)Volume 13, Issue 2
The overview briefs the records of the look for non-Mendelian genes, consisting of the rationale for his or her lifestyles and the methods for their discovery in D. melanogaster. The genes are named ontogenes and their mutations, conditional mutations. Feature functions of conditional mutations in hybridological experiments had been defined. 4 separate sections live at the experimental facts that fairly define the distinction of this novel institution of genes from the classical protein-coding (Mendelian) genes. Specificity inside the function of ontogenes is composed in (1) The warrant that an organism belongs to a selected species; (2) The control of buildings of cell ensembles; (3) The presence of nonchemical (biophysical) way of interplay between ontogenes, as well as the reality that; (4) The mutations in ontogenes as facultative dominant lethals cause the formation of genetic isolates able to trigger the process of speciation.
Conditional mutations; Ontogenes; Mendelian genes; Biophysical interaction of genes; D. melanogaster
The first batch of mutations of this new magnificence became generated in D. melanogaster in 2000 [1,2]. As of today, after almost two decades of the research into these mutations, it is in well-known clean what their variations from Mendelian mutations are and what are the variations of the genes determining these mutations from classical Mendelian genes. The goal of this evaluation is to brief the main experimental records on the so-referred to as conditional mutations and ontogenes, that are chargeable for the formation of conditional mutations, as well as the theoretical generalizations in this lately seemed place of genetics.
The definition of a gene(s) as “new” is regularly met in genetic literature however in phrases of characterization of useful variety of the corresponding proteins coded for through the genes in preference to the genes in step with se. Here, this isn't always the case. We speak approximately virtually new genes which are fundamentally extraordinary from the Mendelian protein-coding genes. At the first look, the examine of this kind have to were accomplished a whole lot earlier, for the duration of the classical length in genetics, when the idea of gene turned into formed. The theoretical situation that interfered with the invention of the genes other than the Mendelian ones will become clear within the route of the narrative. In conjunction with the data about new genes, the overview may be of hobby to the researchers inquisitive about the records of genetics and status quo of the fundamental idea of gene.
Conception of the work
Historically, the examine of the replica of living organisms in phrases of biology from the very starting observed the way of reading inheritance, that is, the transmission of character characters of mother and father to their descendants within the series of generations. Gregor Mendel proposed to take a look at inheritance in the crosses of parents with opportunity characters [3]. The species-level tendencies present as mutually distinct variants are known as alternative. The opportunity characters form the intraspecific diversity of organisms [4,5]. These characters are handy whilst studying the inheritance because they do not prevent crosses of people and give the chance to track the inheritance in any number of generations [3]. The thought via Mendel to observe heredity in line with the inheritance of this class of characters has emerged to be most green, allowing genetics to reach first the level of chromosomes and then, the molecular degree.
The onrush of genetics within the course determined via Mendel and “materialization” of gene as a DNA location containing the code for construction of the corresponding protein brought about the idea that the protein-coding gene is a widespread unit of heredity, the particular familiar thing of heredity the life of which got here to Mendel’s thoughts. The idea of established gene received robust assist from the evolutionary idea of Charles Darwin. Consistent with this idea, the species are the end result of selection of the variations of a trait that offer the very best health of an organism. Accordingly, the presence of versions of a trait in this idea is the pivot with the evolution of the residing “coiling” round it. The tendencies having variants are a sort of the “supply” of dwelling.
However, the species-degree developments are not restricted to the characters which have variations, particularly, there are the tendencies figuring out the intraspecific similarity [4,5]. Any representative of a species possesses such trends. They’re conserved, decide the species-unique appearance and indicate the placement of species in the hierarchy of the living. These traits are inapplicable to hybridological analysis however maximum vital for the genetic concept. The fact that the trends figuring out the intraspecific similarity are conserved indicates that they will be attended with the aid of particular genes. Their specificity consists in that they're prohibited to have variants. The presence of such genes makes it possible to provide an explanation for (1) the lifestyles of a unified software of individual development for all individuals of a species and (2) the incapacity to provide progeny in interspecific crosses; and to create with their assist (three) a brand new model of speciation instead of the cutting-edge one, which does not rise up to scrutiny.
We decided to experimentally verify the speculation at the lifestyles of “different” genes through looking for mutations in those genes. How ought to those mutations seem like? Theoretically, either the prohibition of mutation of a gene accountable for a trait or removal of the acting gene mutation is vital that allows you to offer the consistent presence of similarity in step with the trait in population. The previous assumption looks unreal and the latter demands that the mutant allele is eliminated at once after its emergence, this is, in heterozygote. As for the removal in heterozygote, the simplest risk for new genes to “come into being” is to appear at once in a double dose, this is, in homozygote. This danger should be taken into consideration because in any other case any biological evolution will become unfeasible. Accordingly, a digital portrait of the gene chargeable for a similarity trait is rather extraordinary: the mutations within the gene need to be feasible in a homozygous kingdom however lethal in a heterozygote. The Mendelian gene, with which genetics deals for already over a century, is absolutely antithetical to the brand new gene: The mutations in Mendelian genes are feasible in a heterozygote but deadly (in all instances or frequently) in a homozygote. To check the hypothesis on lifestyles of “other genes”, we decided to look for the mutations paradoxical from the viewpoint of present day genetics, that is, the mutations feasible in a homozygote and deadly in a heterozygote. Once mutations were located, this will prove the lifestyles of the postulated “different genes”.
Generation of mutations
Drosophila is a convenient item when searching for the mutations of hobby. Men bring most effective one X chromosome (and one Y chromosome) and women, two X chromosomes. As a result, men are suitable to test the manifestation of an X-chromosome mutation in a homozygous state and females, in a heterozygous country (in the daughters of a mutant male). D. melanogaster girls had been exposed to γ-irradiation and the progeny of sons and daughters changed into produced. A part of the sons must putatively comprise the goal mutation in the X chromosome. The viability of mutations should be supplied by a homozygous state of mutations. Sons were personally crossed with tester ladies (inside the first experiment, those have been yellow females). The fathers with the absence of daughters (heterozygotes for mutation inside the X chromosome) inside the progeny were appeared as mutants [1,2]. The mutations selected in this way match the planned necessities, i.e., they had been viable in adult males (homozygous for mutation) and deadly in ladies (heterozygous for mutation). The selection pattern, which confirmed its efficacy, fashioned the historical past for other comparable methods of mutation identity [6,7].
The important thing specific characteristic of the used technique is era of the mutations deadly in heterozygote (dominant lethals). However, the very first crosses of the generated mutations proven that the dominant lethality became of a conditional nature. This lethality emerged to be established not best of the mutated gene, however additionally of the general genome in which it become gift. The mutations had been named conditional [6-8], which extensively subtle their definition. As a consequence, those mutations now not only vary within the lethality in homo and heterozygote however additionally the mutations deadly in a single dose (dominant lethality) with their manifestation relying on genotype (facultative dominant lethals). Both functions-dominant lethality and conditional manifestation-determine an essential difference of the generated mutations from the Mendelian mutations, lacking those functions. Moreover, the features of Mendelian mutations are without delay contrary.
The most common situation for manifestation/absence of manifestation of a conditional mutation is the sex of mutant. The situation next in its frequency is the presence of a chromosome rearrangement within the genome. The chromosome rearrangement may be localized (1) within the chromosome opposite to that carrying mutation; (2) within the chromosomes of every other pair; and (three) even within the genome of the associate in pass. Taking into consideration the residences of chromosome rearrangements, we designed the approach to generate conditional mutations in Drosophila chromosome 2. The mutants (each women and men) wearing mutant chromosome 2 together with the other chromosome 2 carrying an inversion survived, while the mutants with everyday opposite chromosome 2 died.
Independently of the phenomenon of dominant lethality, the conditional mutations also own recessive lethality. That is established by using the lethality of homozygotes for mutation in permissive genotypes. Primarily based at the belongings of recessive lethality, we designed the method for choice of conditional mutations from the gathering of recessive lethals in the X chromosome generated in line with Muller-5 take a look at. the selected mutations in the X chromosome occur themselves in adult males as lethals if the preliminary female is crossed with a Muller-five male (as in commonplace stocks) however do no longer show up as lethals if the preliminary lady is crossed with the male without a Muller-five inversion [9].
As became determined out, conditional mutations triggered the development of monstrosities (morphoses) inside the progeny [10,11]. These belongings changed into also used to search for conditional mutations. People with monstrosities were found inside the irradiated flies within the first generation. They have been in addition tested for the presence of recessive lethality. The chosen mutants with showed recessive lethality were cultivated for similarly remark and addition to the list of conditional mutations [7]. The collection of conditional mutations in Drosophila maintained in our laboratory comprised at exceptional instances over 100 of mutations in chromosomes X, 2 and 3.
Properties of mutations in ontogenes
As is mentioned above, the primary experiments with mutants confirmed that the paradoxical lethality, used to pick the mutants, turned into a unique case of an extra primary belongings of these mutations. The lethality in a heterozygous kingdom seems and disappears depending on genetic situations, as an instance, the genotype of the partner in cross. The real fundamental belonging of those new mutations is conditional pattern of their manifestation. The conditional sample of manifestation is what essentially distinguishes them from the Mendelian mutations, which display their unconditional and impartial nature being inherited in keeping with Mendel. The situations for manifestation/absence of manifestation of latest mutations are the genotype of the companion in pass, path of go, sex of person and the presence of a chromosome rearrangement inside the contrary chromosome or the chromosomes of some other pair [6,8].
Genetics is aware about similar mutations, for example, the mutations manifestation of which relies upon on environmental factors, consisting of temperature and meals chemical additives [12]. Another example is the mutations with incomplete penetrance [13,14]. Conditional mutations differ from each variation: From the former type, through changing their manifestation relying on genetic instead of environmental conditions and from the latter, via that the manifestation or absence of manifestation is strictly related to precise genotypes. A strict affiliation with particular genotypes is untypical of the mutations with incomplete penetrance.
Even though conditional mutations may have a visible manifestation, the so-called dimorphic mutations, the fundamental manifestation is conditional (facultative) dominant lethality. Facultative dominant lethality is observed via obligate recessive lethality. The latter appears in the mutants with permissive genotypes, in which dominant lethality is absent. Recessive lethality makes it possible to check mutations for allelism and, which is essential, demonstrates a discrete individual of the genes answerable for mutations. Using a trendy technique of deletion mapping, we localized the mutations manifesting recessive lethality on the map of polythene chromosomes. This mapping discovered an uncommon phenomenon of multilocality: Of the 10 examined mutations in chromosome 2, 5 mutations have been localized to two and extra chromosome 2 areas [15].
Characteristic of the mutants is a strangely extensive time c language while mutations appear themselves in the Drosophila lifestyles cycle. Their manifestation in the soma within the form of the so-referred to as morphoses, complicated somatic monstrosities, is astonishing. This kind of manifestation counseled us to consult the genes responsible for those mutations as ontogenes [16,17]. Mutations additionally happen themselves within the germline tissue. They set off meiotic abnormalities via extensively increasing the charges chromosome nondisjunction and loss [18].
Ontogenes differ from Mendelian genes with the aid of their interest for the duration of premeiosis. With none exclusions, all manifestations of ontogenes, be it lethality and its modifications or development of morphoses, observe a parental type of inheritance [19]. The parental type seems in special forms (maternal, paternal, mixed or nonreciprocal). Parental inheritance suggests that a product is shaped in premeiotic cellular with a view to be allotted with the development of meiosis independently of the gene that gave rise to it [20]. The maximum brilliant and earlier unknown asset of the mutants is that they show a multiplied level of fundamental metabolism and locomotor interest.
This summary of the houses of conditional mutations show that they constitute the genes basically extraordinary from Mendelian genes. See for the residences of conditional mutations in extra element. Presently, the content material of the term “ontogene” has much in common with the term “long noncoding RNA genes”, which appeared in molecular genetics [20]. Inside the sections underneath, we continue to keep in mind the properties of ontogenes via grouping complexes of the residences because the arguments in choose of specific organic missions of ontogenes.
Facultative dominant lethals are a new type of genetic mutations
In terms of modern genetics, the major part of the generated mutations may be referred to as Facultative Dominant Lethals (FDLs). Genetics lacks the category of mutations thus named. Hadorn asserts the existence of two categories of lethal mutations, namely, (1) the dominant mutations with a recessive lethal effect and (2) the recessive lethal mutations without a dominant effect. In Drosophila, the first category comprises the mutations with a visible dominant manifestation, such as Curly, Lobe and Dichaete, unable to exist as a homozygote. As for the second category, it unites the mutations that do not manifest themselves a in a heterozygote but appear lethal in a homozygote. They are referred to as recessive lethal mutations. After Muller used them in the experiments on radiationinduced mutagenesis, they became the most frequently used type of mutations for testing the mutagenic effect.
In our experiments, the rate of FDL generation in Drosophila does not yield to the frequency of recessive lethal mutations [2] and exceeds the latter in the originality of manifestation and significance. The lethalality of FDLs suggests a high importance of a mutated gene (ontogene). Its alteration even at a single dose is mortal for the corresponding individual. The facultative manifestation suggests that the corresponding gene belongs to some class of genes other than the Mendelian genes since characteristic of the latter is an obligatory manifestation. In addition to the facultative manifestation, FDLs induce genome instability and formation of isolate comprising mutant individuals. Find below a more comprehensive description of these specific features.
Facultative manifestation (in other words, the dependence of manifestation on genetic conditions) is not characteristic of the Mendelian genes. The Mendelian genes are an example of the full and unconditional relation adherence to “gene–trait” scheme. The rules of inheritance of traits (Mendelian inheritance) cannot exist without the strict gene–trait relation. The fact of facultative manifestation of FDLs fundamentally distinguishes the ontogenes from Mendelian genes and demonstrates that a separate control machinery (controlling subsystem) exists within the overall genetic system. Thus, ontogenes are in control of the operation of Mendelian proteincoding genes. The unique properties of the subsystem composed of ontogenes will be described below.
Genetics encountered individual examples of facultative gene manifestation as early as the classical period of its development but failed to understand this anomaly. A conditional manifestation was ascribed to the fact that a trait was multigenic and was formed in several stages. This explanation was prevalent at the stages of both formation of the terms expressivity and penetrance [13,14] and the debate on the mechanisms underlying ontogenesis. The failure of this interpretation is currently evident. The traits with involvement of Mendelian genes are also multigenic and multistep but still display the obligatory manifestation adhering to the Mendelian rules rather than a facultative manifestation pattern. The true cause underlying the facultative manifestation, the property seemingly quite foreign to genes, became clear when it appeared that this property (facultative manifestation) was not a certain exotic feature but rather characteristic of the entire category of ontogenes.
The cause underlying the “manifestation–nonmanifestation” for the ontogenes as the control genes is not only the state of a control gene itself, but also the state of its connections with other control genes and the states of these control genes. The facultative manifestation of ontogenes suggests at least the most important points: (1) the existence of gene interaction (regulation); (2) the existence of alternative routes in regulation; and (3) the ability of ontogenes to remain in an off-mode during the entire life of an individual. All these characteristics are untypical of the Mendelian genes.
Induction of instability: Hadorne in his monograph titled developmental genetics and lethal factors defines mutation with the reference to Muller as a change in genetic material that transforms a certain relatively stable state into another relatively stable state; the new state is reproduced in hundreds of thousands of cell generations. Thus, a “stable state” of a gene after mutation is emphasized. Current genetics commonly and by default regards mutations as stable despite the recognized fact of genetic instability phenomenon.
Current genetics knows numerous examples of instability; its molecular mechanism is known; however, the biological meaning of the transition from stability to instability and the “goals” of this transition are yet vague. The role of ontogenes for understanding the phenomenon of instability cannot be overestimated. Instability appears a common event occurring with the ontogenes programmed by the genetic system itself and used as a tool. The association of genetic instability with FDLs may well mean that instability is the response to a mutation in an ontogene. As for the meaning of instability, it consists in the restoration of the control over the operation of genetic system by ontogenes in the previous form or in some other variant.
Formation of genetic isolate: The event of generation of a single FDL changes the population-level relationships of its individuals. The lethality of an FDL is incomplete; correspondingly, this produces a group of the offsprings carrying the FDL. This subpopulation among the individuals lacking the FDL is an isolate. The fact of isolation is confirmed by systematic death of the offspring in the crosses with FDL+ and FDL– individuals. The high genetic instability caused by the presence of FDL (see the previous section) makes the isolate distinct. Consequently, the isolate becomes the reservoir of new genetic variants. However, the isolation is partial. As is assumed, the size of an isolate and the degree of isolation can change. The isolate can disappear or form the background for a new specieslevel taxon.
Unlike the conventional Mendelian mutations, which do not interfere with the panmixia in population in principle, FDLs do interfere with the panmixia and in a hidden manner prepare the population to the formation of a new species. The outstanding role of FDLs in this process results from the specificity of ontogenes. These control genes not only compose the constantly working program of individual development, but also are able to recreate this program. The ability of ontogenes to provide the relationship between genetic elements is quite expectable and the demand in control genes to guarantee the operation of genetic system has been repeatedly asserted. However, the ability of ontogenes to segregate the population into isolated entities and to organize mutagenesis in one of them is an unexpected surprise.
The considered features of FDLs demonstrate that a new star (factor) with the earlier unknown specific features but most important capabilities rises in the genetic firmament. The capabilities are determined by that the ontogene in terms of function represents not only itself (as is the situation with the Mendelian gene), but also the genetic structures connected with it via the program of individual development.
Ontogenes determine species attribution
The manifestation of mutations in ontogenes offers a touch on the functions function of distant hybridization, i.e., crossing of individuals that belong to unique taxa (species, genera, families and so on). Hybridization is followed by using the common picture of abnormalities impartial of a specific go and the kingdom, plant or animal, of the dad and mom. The sample of abnormalities (as inside the sample of interspecific incompatibility) includes (1) high sterility of crosses; (2) parental effect whilst producing the hybrid; (3) mosaicism and improvement of monstrosities in the hybrid; and (4) the meiotic abnormalities within the hybrid main to sterility.
The generated ontomutations (mutations in ontogenes) in Drosophila also display:
Sterility of crosses: Ontomutations are conditional dominant lethals. The progeny in the crosses with ontomutations may be absent in any respect or in element.
Parental type of inheritance, which is an ordinary shape of inheritance of the manifestations of ontomutations. Ontomutations display one of kind sorts of parental effect each hardly ever met or absent in any respect when managing Mendelian mutations, consisting of paternal and combined paternal–maternal kinds of inheritance. For complete description of the varieties of parental impact, see [19].
Mosaicism and development of monstrosities (morphoses): Mutants for ontogenes regularly develop mosaic sites. Monstrosities (morphoses) in mutants are some of the most hanging manifestations in mutants. The improvement of morphoses is defined via Sokolov for the hybrids between D. virilis and D. littoralis in reciprocal crosses.
Meiotic abnormalities: Extremely high prices of the Xchromosome nondisjunction in meiosis are recorded for 30 ontomutations [18]. The proportion of matroclinous daughters for the X-chromosome reaches 24.7% of the general progeny. Similarly to nondisjunction, the X chromosome is lost and a part of nondisjoined X chromosomes is change chromosomes. An excessive charge of X-chromosome nondisjunction in Drosophila girls indicates a trend of inheritance in daughters. This information advises a profound disease of the meiotic division inside the mutants for ontogenes [18].
As is obvious, the sample of abnormalities in ontomutants is much like the sample of interspecific incompatibility. We can't help however wonder what motive is underlying incompatibility. Heterozygosity for Mendelian genes can't be the cause of incompatibility because it does no longer lead to lethality; moreover, it often leads to hybrid vigor, heterosis. In addition, mutations in Mendelian genes do now not intrude with meiosis and they may be feasible even within the compound with a deletion. It’s far clean that the heterozygosity for Mendelian genes cannot be accountable for interspecific incompatibility. Correspondingly, we will think that the purpose underlying incompatibility is the heterozygosity for the genes that decide species attribution. In their native genome, these genes are in a homozygous state, which allows them to correctly perform their project.
The observed similarity among the manifestation of ontomutations and the pattern of interspecific incompatibility in distant hybridization permits us to infer that (1) ontogenes belong to the institution of genes liable for intraspecific similarity and (2) the uncommon phenomenology of ontomutations is resulting from their heterozygosity for ontogenes. The latter is akin to the heterozygosity in remote hybridization but is attained in a one of a kind way. Ontomutations are acquired by mutagenesis, whereas the heterozygotes for an ontogene emerge in the hybrids among ordinary individuals and mutants. Certainly, we need to remember that all genes responsible for species attribution are in a heterozygous country in an interspecific hybrid and in the experiments with ontomutations, handiest one gene (ontogene).
The determined similarity to the pattern of interspecific incompatibility considerably simplified the expertise of the position of ontogenes in the organism. “Incompatibility” does no longer exist for Mendelian genes. Interspecific incompatibility is the conflict of the genes that shape the species-degree specificity of the organisms and ontogenes, mainly, are these genes. Simply deliver returned to thoughts the pattern of incompatibility in remote hybridization and the position of ontogenes is clear.
Ontogenes control the process of building cellular ensembles
Among all manifestations of the mutations in ontogenes, a group of five manifestations indicates that ontogenes manage building cell ensembles. While speak me about the manage of constructing cell ensembles, we mean (1) an occasion in ontogenesis that (2) consists in initiation of cell department and (three) fixes the position of cell department aircraft, which determines the growth route of cell mass. This institution of 5 manifestations comprises the phenomena of (1) development of morphoses; (2) parental form of manifestation of a morphosis in progeny; (3) asymmetry of morphoses; (4) disturbance of cell meiotic department: and (5) disturbance of cellular mitotic department.
In genetic literature, morphosis (monstrosity) is defined as a “nonadaptive and commonly risky variant in man or woman morphogenesis related to a trade in environment”. In our case, morphosis is an inheritable morphological abnormality caused by a mutation in an ontogene. The genetic nature of morphoses is clear from a parental type of their development inside the progeny of a mutant. Each the progenies that obtained the mutant ontogene from the determine and the progenies that did now not get hold of the mutant ontogene can also expand morphoses. As a consequence, it is clean that the emergence of a morphosis isn't a sure “physiological aberration” of the ongoing ontogenesis but rather the end result of a trade within the genetic application of development that occurred lots time ago inside the determine’s germline.
The phenomenon of parental “inheritance” of a morphosis is likewise crucial in any other recognize. As is mentioned above, parental inheritance is a hallmark of the gene pastime in premeiosis. The Mendelian genes are inactive in premeiosis (in germline cells) and the protein synthesis is absent. This suggests that neither protein molecules nor protein-coding genes have whatever to do with the formation of colossal structures. The question arises on how do ontogenes implement this. The phenomenon of asymmetry of morphoses offers the solution.
Morphoses appear themselves in methods: as a “+ tissue” (outgrowths) and as a “– tissue” (the absence of normal systems). The phenomenon of asymmetry of morphoses is composed within the reality that the morphoses of each kinds appear on best one aspect (right or left) of the fly frame, while their ordinary analogs are bilaterally symmetric structures (wings, legs and so on). The presence of an odd shape, as an instance, at the left aspect and its absence at the proper aspect way that a mutant ontogene brought about a series of successive mobile divisions at the left frame facet, which did not take region at the right aspect. The target for the motion of ontogene is cell. This agrees with the above conclusion that protein is not implicated within the emergence of morphoses.
In modern genetics, protein, be it structural or regulatory, is seemed as the handiest organic manufactured from gene. In contrast to the Mendelian genes, the fabricated from pastime of ontogene is mobile. Mendelian gene creates protein de novo from precursors, whereas ontogene creates a new mobile by means of initiating division of a precursor cellular. In the case of morphoses, it seems that ontogene not best initiates mobile division, however additionally determines the aspect of the frame where it should be performed.
As is known, the mutations of Mendelian genes also are able to result in morphological defects. But, word that these defects, unlike the morphoses, are usually symmetric and are inherited in step with the policies of Mendel as opposed to in line with a parental type. Therefore, its miles clean that the Mendelian protein-coding genes cannot faux to govern cell construction.
Different phenomena, indexed at the beginning of this section, additionally verify the implication of ontogenes in cellular construction, particularly, the abnormalities of meiotic and mitotic divisions. Extraordinarily high charges of chromosome nondisjunction and chromosome loss without delay imply disturbances of meiosis [18]. Be aware that an unmarried dose of mutation causes an increase in chromosome nondisjunction. Mitotic cellular division is also disturbed in the mutants for ontogenes, as is recommended via the formation of mosaics and gynandromorphs in those mutants. As is thought, factor mutations in Mendelian genes do not intervene with either meiotic or mitotic mobile division.
The totality of the located phenomena makes it viable no longer best to deduce that ontogenes are engaged in cell production, however additionally to get the perception into the information in their involvement on this technique. The phenomenon of asymmetry demonstrates that ontogenes are able to orient the forming mobile in three-dimensional area (1) leftward or rightward, (2) upward or downward or (3) forward or backward. This activity may be finished if the event of cellular division initiation is followed by means of willpower of the department plane. Three positions on this aircraft are enough to decide the increase of mobile mass in (1) anterior–posterior, (2) lower–top or (3) lateral instructions. Assuming that ontogenes are capable of “count cell divisions” from the moment of zygote formation, this system of individual improvement is sort of ready. The pastime of ontogenes in premeiosis can be seemed as proof of exceptional-tuning (editing) of this application in germline cells.
The experimental paintings with mutations of ontogenes frequently call for the usage of fly shares containing Mendelian mutations. The manifestation sample of Mendelian mutations on the historical past of morphoses may be very interesting: The Mendelian mutations continue to commonly take place themselves even within the structures that are altered through morphoses and lost their symmetry and typical region at the body. This indicates that the frame plan of a selected species is decided by way of ontogenes and ontogenes exceptional-music Mendelian genes to this frame plan. We trust that the program of character development includes sequentially switched-on ontogenes. Triggering cellular divisions, ontogenes construct the cellular framework for the future organism. In strict accordance with this system of man or woman improvement, ontogenes activate Mendelian genes within the newly fashioned cells. For simplicity, the details related to the cellular segregation into stem and differentiated ones are disregarded from this scheme.
Biophysical nature of ontogene activity
The ability to govern cell production functionally distinguishes ontogenes from Mendelian genes, involved in protein synthesis. It’s far logical to assume that this distinction can be prolonged to the genetic style of gene operation as nicely. The experimental statistics verify this expectation: Ontogenes (1) engage with their own type in a remote manner; (2) are energetic in a compact nation; and (three) show up the so-called paradox of homologous pairing. Such manifestations are unobservable for the Mendelian genes.
Remote interplay of ontogenes: Meiosis begins from pairing of homologous chromosomes. The upcoming of homologs is supplied by using the interaction of homologous genes. In advance, it became believed that the interacting genes have been Mendelian genes; but, it has emerged that those genes are ontogenes. This is proven by way of high costs of nondisjunction of homologous chromosomes within the mutants for ontogenes [18]. Noteworthy that here we talk about a remote interplay, that is, the interplay inside the absence of a physical touch between them. Another example of remote interaction is the interplay among parental pronuclei after fertilization. This interaction is blocked in part of zygotes; pronuclei fail to approach one another; and zygotes die before starting to broaden.
Pastime of ontogenes inside heterochromatin: The chromosome cloth in a dividing meiocyte is in a compact nation. Correspondingly, the ontogenes that provoke pairing of homologs accomplish their pastime being in a compact nation. The pastime of ontogenes in a compact nation is likewise confirmed with the aid of the pathology within the interaction of pronuclei in the zygote, as is stated above. As is understood, the chromosomes within gametes also are pretty compacted. Consequently, we may country that the chromosome cloth display its interest no longer most effective in an uncoiled state (Mendelian protein-coding genes for the duration of protein synthesis), but additionally in a compact nation (ontogenes) [18].
Paradox of homologous pairing: Evaluation of an event of meiotic pairing related to the homologs considered one of which includes an inversion noticeably demonstrates that the upcoming of homologous ontogenes is unbiased of the mutual positions in their sequences in space. Because of this the nucleotide sequences of ontogenes are capable of engage (1) at a distance and (2) independently in their mutual positions in space.
All 3 specific capabilities are logically interconnected and all three advise that ontogenes function in a way one-of-a-kind from Mendelian genes no matter their chemical kinship. The remote interaction independent of mutual positions of nucleotide sequences in area at once leads to the conclusion that the interplay is of a bodily nature (thru formation of a physical, say, electromagnetic, subject) rather than of a chemical one. The putative compaction of active ontogenes perfectly suits an electromagnetic nature of the interplay. Similarly, be aware that the formation of a three-dimensional shape, which a multicellular organism is, calls for a spatial orientation of the fashioned new cells and that is unfeasible without a certain spatially oriented outside field and the genetic elements able to linking them to the 3-dimensional spatial function.
Blyumenfel’d postulated the lifestyles of DNA magnetic residences in his experimental works as early as 1959. The stacks of DNA bases were proven to be properly conductors inside the experiments on assessing DNA electrical conductance. The stacks show off semiconductor properties and may transfer holes and electrons. The formation of chemical bonds of a sure kind known as resonance bonds (an example is benzene molecule) creates a specific scenario while a few electrons turn out to be delocalized and for that reason able to freely journey throughout the entire molecule. The delocalized pi-electrons or delocalized protons of the hydrogen bonds in DNA can migrate in order that a stack of nucleotide bases acquires the properties of an isolated conductor, whilst the DNA strand on nucleosomes turns into an inductance coil that generates a magnetic discipline. In line with Myakishev-Rempel et al., some of nucleosomes with a DNA place form an oscillatory circuit that creates an oscillating magnetic field. The DNA regions that shape the oscillating magnetic subject are capable of set off the oscillation of the DNA regions comparable or near of their molecular shape. The lifestyles of a resonance interaction between DNA areas become assumed to explain the phenomenon of technology of whole mutations by way of radiation impact on double-stranded DNA.
But, this new biophysical hobby kind, as some distance as we recognise, is not the only one for ontogenes. The dominant lethality of ontogenes indicates that their pastime modifications depending on the presence in the genome of chromosome inversions in a heterozygous country [9]. The impact of inversions follows a parental type; this fact demonstrates that ontogenes are active in premeiosis. This form of interest excludes their involvement in protein synthesis, as is referred to above, however do no longer observe the pastime related to a physical discipline as well. The activity related to the sphere cannot rely on the rearrangement of spatial positions of the interacting items. Correspondingly, we need to anticipate that the hobby of ontogenes in germline cells consists inside the production of small nuclear RNAs. As a consequence, ontogenes are putatively in a position to accomplish styles of activity, specifically, a biochemical one utilizing small nuclear RNAs and a biophysical one, using wave pastime. The primary variant is implemented in germline cells at the same time as modifying the program of man or woman development and the second one, all through implementation of this software within the growing soma.
We can't however point out a number of theoretical troubles resolvable in phrases of the biophysical (area-based totally) doctrine but irresolvable in terms of the chemical doctrine. The chemical doctrine, postulating the law (manage) through individual chemical substances, admits simplest a stepwise manage. As for the sector-primarily based doctrine, it allows for advent of complicated multivector signals with the assist of interference. These multivector signals permit spatial ensembles of systems to be built. It is essential to remember that the idea of basically controlling the protein synthesis with the help of protein regulators is first of all inadequate because a protein regulator requires its very own protein regulator and with no end in sight, which is inadmissible for a actual existence concept.
Ontogenes and other biological problems
Ontogenes and only ontogenes have allowed the three biological problems considered above-(1) intraspecific similarity, (2) cellular construction and (3) biophysical interaction-to appear in the area of genetics. However, ontogenes are also pertinent to the problems raised as early as the Mendelian genetics. A novel view on some problems traditional for genetics, namely, in terms of a two-component genome comprising the Mendelian proteincoding genes and ontogenes, gives the chance to resolve these challenges. Below, we will dwell on some problems.
Biological trait: Genetics started from the assertion that any biological trait was determined by hereditary factors (genes). Many genes can be involved in this process (multigenic traits), as well as two genes (digenic trait, digenic cross) or only one gene (monogenic trait, monogenic cross). Our data on the control of cellular construction by ontogenes define a biological trait either as a morphological structure composed of cells or as a function of a cellular structure. As such, the trait appears as part of the organism of its particular species and can be compared to the corresponding traits of organisms belonging to other species. In this standpoint, any biological trait is multigenic. Even in the limiting case, it is controlled by at least two genes: An ontogene responsible for emergence of a cell and a Mendelian gene responsible for production of a protein. All the remaining definitions and classification of traits (qualitative, quantitative, monogenic and polygenic) are artificial and provisional and may be useful only for certain specified situations. The old terms “monogenic” and “polygenic” are also admissible but only with a distinct understanding that they refer not to biological traits but rather to variants of these traits that are determined by the defects of one, two or more genes (ontogenes or Mendelian genes).
Ontogenesis: The process of individual development of a living organism follows a unique program characteristic of only this species and no other one. The role of protein-coding genes is known and is not discussed; however, the protein-coding genes can vary and this excludes the possibility to consider Mendelian genes as a warrantor of uniqueness and conservation of the individual development program for a species. The uniqueness and conservation are determined by ontogenes. Thanks to their ability to provide a lethal effect in heterozygote, ontogenes demonstrate both the very fact of uniqueness of the program of individual development and the mechanism that underlies the maintenance of conservation of this program within a species [11].
Phylogenesis: The current evolutionary genetics in the form of the modern evolutionary synthesis assigns the primary importance to the selection of alleles of protein-coding genes. Darwinian selection provides for the best fitness of an organism. This interpretation of the evolutionary process is wide open to criticism since the living organisms of the overall “ladder of life” starting from the most primitive ones until now display an excellent fitness. This fact discredits the very idea. Once the brunt of the problem is shifted to ontogenes, this withdraws the main objection against the theory of selection. Darwinian selection for fitness at the level of adult organisms does take place but this is not the chief factor in the evolutionary process. The chief is the selection of ontogenes and their ensembles in the zygote when the chromosome sets of the parents met. It is the zygotic selection that leads to a change in the genetic program of individual development. The very same selection forms the mechanism underlying the isolation of a nascent species
The paramount role of ontogenes in the evolutionary process for the first time solves the mystery of a special evolutionary pattern characteristic of unicellular organisms. Similar to multicellular organisms, cell is their component and they possess DNA and genes, that is, all ingredients allowing them to evolve according to the Darwinian scheme of selection for better fitness. However, unicellular organisms do not show any evolution at least in the variant that is regarded as evolution by biologists. They divide but do not form complex cellular constructions. It is reasonable here to assert that they even have no tools for this purpose, first and foremost, the specific genes (ontogenes) capable of cellular construction in a threedimensional space.
The advance in genetics in many respects relies on the use of unicellular organisms in genetic experiment. Universality of the genetic theory for all living things is constantly emphasized. This paper identifies itself with the modern inheritance theory utilizing the concept of genes but leads to the conclusion on the fundamental difference in the gene composition of unicellular and multicellular organisms. The former lack both ontogenesis and ontogenes. The latter has ontogenesis and ontogenes. The data on the functional biological role of ontogenes unambiguously suggest that ontogenesis and phylogenesis are the problems associated with multicellular organisms rather than with the all living. The main content of both is the construction of cell ensembles with the help of genes and ontogenes. The statements on a special place of the unicellular organisms in the world of all living things deserve careful attention. The format of this review does not allow us to consider this issue in detail; however, its title purposefully attracts attention to the tight association of the research into the new gene category with the most important problem in biology, namely, the issue of unicellularity and multicellularity.
Mutagenesis: The evolution of the living demands that gene material is mutated. For mutations to occur, this material must be in an active state. If we consider protein-coding genes alone, active only during somatic development, all or the overwhelming majority of formed mutations die together with their owners without being passed to the offspring. Thus, it is reasonable to ask where and when mutations (without which any evolution in impossible) are formed.
The experiments with mutations of ontogenes directly indicate the source and time moment when mutations are formed, namely, in the DNA in the germline. The DNA activity is suggested by inheritance of the manifestation of conditional mutations according to a parental type. The parental type of inheritance (in a broad sense) emerges if a gene is active before meiosis and produces the gene product that loses the link with the gene that gave birth to it. The gene material in the germline acquires the status of “active” thanks to ontogenes. The Mendelian protein-coding genes in germline cells are inactive. Thus, genetic instability, transposition of mobile elements, hybrid dysgenesis, epigenetic transformation and “genome editing”, taking place during gametogenesis in the germline, can be rightly regarded as the events involving ontogenes.
Inbreeding depression and heterosis: Inbreeding in animals and plants leads to formation of weak progeny with a low fertility (inbreeding depression). An opposite phenomenon is the formation of strong and highly fertile progenies exceeding their parents (heterosis). The latter phenomenon is observable in the crosses of the remote relatives of the same species. The hypotheses on the mechanisms underlying inbreeding depression and heterosis are similar in that the cause is of a genetic nature. The difference is in the degree of homozygosity of the genome, which is maximal in the case of inbreeding depression and minimal in heterosis. However, the mechanism that would explain how the level of homozygosity influences the habitus of progeny is so far vague. The phenomena of heterosis and inbreeding depression are already referred to as “a challenge to genetics”.
The very fact that ontogenes exist makes it possible to explain these phenomena. Thanks to ontogenes, genome emerges to be two-component, comprising the classical Mendelian genes and ontogenes. In the genome of a species, ontogenes are in a homozygous state. The procedure of maximal heterozygotization of the genome (production of hybrids of highly inbred parents) should lead to the situation when homozygous ontogenes are on the background of heterozygous Mendelian genes. The resulting contrast may enhance the recognition and switching on of homozygous ontogenes (the phenomenon of heterosis). On the contrary, the procedure of homozygotization of the genome should conceal the locations of homozygous ontogenes among similarly homozygous Mendelian genes. This may complicate the recognition and switching on of ontogenes (the phenomenon of inbreeding depression). The earlier hypotheses focused on different modes of function of a one-component genome as the cause of these phenomena and alas, failed. As for our postulated hypothesis, the underlying cause consists in a two-component composition of the genome and the influence of the genes of one type on the function of the genes of the other type as early as the recognition of sequences.
Our research continues the classical genetic studies started by Mendel and actively performed now. Our work could not succeed without regard to the role of DNA in heredity and the knowledge about chromosomes and protein-coding genes. This information inspired the idea of the work and assisted in the interpretation of results. However, our research made a sharp turn from the beaten path in genetics, which focused on studying the genetics of alternative characters. In this way, we discovered the genes other than Mendelian ones, namely, ontogenes. In turn, ontogenes have made it possible to reveal the incompleteness of biological knowledge, based exclusively on Mendelian protein-coding genes. It has become clear that the genetic research until recently has dealt only with the traits specifying intraspecific differences, omitting the traits that determine intraspecific similarity, which include the fundamental characteristics of the living. Until recently, only a protein side of the biological traits has been available for genetic research, whereas a cellular side or in other words, the cellular architecture of organism, remained on the sidelines. The new genes, ontogenes, will assist in filling in these gaps in genetic knowledge and the advance in the ontogenetic and phylogenetic issues, waiting long for their resolution.
The results of our work give rise to reasonable doubt in the universality of the chemical modus operandi of genetic machinery. Some new facts favor a biophysical interaction between genes (kind of electromagnetic field–based interaction). The field-associated interaction in inanimate nature is a routine event and the fact that it is absent in the current genetic knowledge about animate nature does not look rationale. Our results and the changes in the energetics of the mutants for ontogenes also suggest the existence of field-associated interaction.
This research was founded by the Ministry of Science and Higher Education of the Russian Federation via the Institute of Cytology and Genetics, Siberian Branch, Russian Academy of Sciences (no. FWNR-2022-0015) for the microdissection and FISH analysis. The microscopy was performed at the Core Facility for Microscopy of Biological Objects, the Institute of Cytology and Genetics SB RAS (reg. no. 3054), Russia.
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Citation: Chadov BF, Fedorova NB (2025) A New Class of Genes in Multicellular Organisms: The Case Study of Drosophila. J Curr Synth Syst Biol. 13:107.
Received: 07-Mar-2024, Manuscript No. CSSB-24-30049; Editor assigned: 10-Mar-2024, Pre QC No. CSSB-24-30049 (PQ); Reviewed: 22-Mar-2024, QC No. CSSB-24-30049; Revised: 09-Apr-2025, Manuscript No. CSSB-24-30049 (R); Published: 16-Apr-2025 , DOI: 10.35248/2332-0737.25.13.107
Copyright: © 2025 Chadov BF, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.