Synthesis Of New RNA Research Articles

Plasmodial incompatibility in the myxomycetes: a review

Two myxomycete phaneroplasmodia of the same species undergo somatic fusion only if they are phenotypically identical for a complex genetic incompatibility system. This system consists of a three tiered polygenic complex with dominant and recessive alleles. Thus, plasmodia must be phenotypically identical for approximately 16 loci in order to fuse (CC and Cc are phenotypically identical, but different from cc). The first level of the system (having a minimum of seven Fus loci) controls membrane fusion, and it apparently prevents fusion unless the two plasmodia have identical membrane or slime sheath components. The second level (having a minimum of six Cz loci) produces a rapid lysis of a small mixed region, of the two plasmodia, if membrane fusion has occurred. This lysis is directional in that it targets the recessive phenotype, and it is apparently triggered by some pre-formed substances when they come into contact with a different plasmodium. The third level (having a minimum of three Let loci) comes into play if membrane fusion occurs and there is no rapid lysis of the mixed plasmodium. It produces a slow lethal reaction, which targets and degrades the nuclei of the recessive phenotype. This reaction occurs over a period of five to twenty hours and requires the synthesis of new RNA and proteins. Since, this complex system produces a minimum of 65,536 different incompatibility phenotypes, it is highly unlikely that any two phaneroplasmodia will undergo a successful fusion unless they are very closely related. Species with aphaneroplasmoida apparently have a similar system, but species with small protoplasmodia do not appear to undergo any type of plasmodial fusion.

Mechanisms for programmed cell death in the nervous system of a moth.

In the moth Manduca sexta 50% of the abdominal motor neurons and interneurons die during the first days after the adult emerges. Although the dying motor neurons innervate larval muscles that also die at this time, the death of the neurons has been shown to be a direct response to an endocrine signal, the decline in ecdysteroids that occurs at the end of metamorphosis. The response to the withdrawal of the hormone apparently requires new synthesis of RNA and protein, as actinomycin-D and cycloheximide can prevent neuronal death. This selective neuronal death probably results from changes in gene activation. The fixed spatial and temporal pattern of neuronal death, however, suggests that trophic interactions among neurons may also be involved. Current work is focused on the fate of a pair of motor neurons, the MN-12 cells, in the third abdominal ganglion. Isolation of this ganglion from the thoracic ganglia can prevent the death of these cells at the time when they would normally die in response to removal of ecdysteroids. The factors mediating this effect may act in concert with the ecdysteroid decline to specify the exact time of death for individual neurons.

Early Contact Stage of Apoptosis: Its Morphological Features and Function

Apoptosis has been a biological phenomenon of intense interest for 20 years, but the earlier morphological features of apoptosis have not been determined hitherto. Using the methods of semi- and ultrathin sections, the livers of intact embryos and young rats have been studied under the effect of cycloheximide to determine morphological features of an early stage of apoptosis. It is discovered that both in hepatoblasts and hepatocytes, apoptosis, besides the well-known stages, also includes an early contact stage, distinguishing features of which are agglutination of bound ribosomes (breaking of translation), elimination of the nucleolus, reduction of free polysomes (and in hepatocytes, reduction of cisterns of rough endoplasmic reticulum), formation of cytoplasmic excrescences, and cell shape changes. The early stage of apoptosis is characterized by close contact with neighboring cells. At a certain phase of the contact stage of apoptosis, the nucleolus reappears in the nucleus and the number of free polysomes in the cytoplasm increases, which suggests the renewal of synthesis of new RNA and proteins. Close contact of differentiating and mitotic hepatoblasts with apoptotic cells indicates a certain functional relationship between these cells that is realized not only by micropinocytosis, but through gap junctions as well. We assume that the apoptotic cell, besides proteolytic products, can contain newly synthesized, low-molecular substances, the relocation of which from apoptotic to neighboring cells may contribute to both functional activity and proliferation of adjacent hepatoblasts and, therefore, the function of apoptosis may not be limited only to the elimination of harmful, damaged, and unwanted cells.

Restoration of Resistance to Osmotic Swelling of Vitrified Mouse Embryos by Short-Term Culture

In cryopreservation of mammalian embryos, embryos can be injured by osmotic swelling during removal of the cryoprotectant after warming. We have shown that vitrified embryos are more sensitive to osmotic swelling than fresh cells but that sensitivity is reduced or abolished if vitrified cells are cultured for a short period before subjecting them to hypotonic stress. In the present study, we examined the mechanism by which vitrified two-cell mouse embryos regain their resistance to osmotic swelling by culturing the embryos in the presence of various inhibitors before hypotonic treatment. New synthesis of RNA and proteins during culture was not required for regaining resistance to osmotic swelling because actinomycin D and cycloheximide failed to inhibit restoration. Inhibitors of polymerization of microfilaments and microtubules (cytochalasin B and demecolcine, respectively) also did not affect restoration of resistance to osmotic swelling, suggesting that rearrangement or repolymerization of cytoskeletal components is not involved in this process. On the other hand, brefeldin A and concanamycin A, which inhibit intracellular vesicular transport, strongly suppressed restoration of resistance. These results suggest that the intracellular vesicular transport system plays a crucial role in restoration of resistance of vitrified embryos to osmotic swelling during short-term culture.

Brief theta-burst stimulation induces a transcription-dependent late phase of LTP requiring cAMP in area CA1 of the mouse hippocampus.

Memory storage in the mammalian brain can be divided into a short-term phase that is independent of new protein synthesis and a long-term phase that requires synthesis of new RNA and proteins. A cellular model for these two phases has emerged from studies of long-term potentiation (LTP) in the three major excitatory synaptic pathways in the hippocampus. One especially effective protocol for inducing robust and persistent LTP is "theta-burst" stimulation, which is designed to mimic the firing patterns of hippocampal neurons recorded during exploratory behavior in intact awake animals. Unlike LTP induced by non-theta tetanization regimens, little is known about the biochemical mechanisms underlying theta-burst LTP in the hippocampus. In the present study, we examined theta-burst LTP in the Schaffer collateral pathway. We found that 3 sec of theta-burst stimulation induced a robust and persistent potentiation (theta L-LTP) in mouse hippocampal slices. This theta L-LTP was dependent on NMDA receptor activation. The initial or early phase of theta-LTP did not require either protein or RNA synthesis and was independent of cAMP-dependent protein kinase (PKA) activation. In contrast, the late phase of theta-LTP required synthesis of proteins and RNA and was blocked by inhibitors of PKA. Prior induction of theta-LTP also occluded the potentiation elicited by chemical activation of PKA. Our results show that, like non-theta LTP, theta-induced LTP in area CA1 of the mouse hippocampus also involves transcription, translation, and PKA and suggest that cAMP-mediated gene transcription may be a common mechanism responsible for the late phases of LTP induced by both theta and non-theta patterns of stimulation.

Interleukin-2 prevention of apoptosis in human neutrophils.

Evidence is presented that interleukin (IL)-2 maintains viability of human polymorphonuclear cells (PMN) in culture by preventing these cells from undergoing programmed cell death (PCD) and induces the synthesis of new RNA and protein. Our laboratory has recently discovered that human PMN constitutively express IL-2 beta receptor and more importantly, PMN are able to respond functionally to IL-2 by enhanced growth inhibitory activity against an opportunistic fungal pathogen, Candida albicans. We now report that IL-2 was able to interfere with the PCD process and reduce the number of apoptotic PMN to < 40% in 72-h culture. Freshly isolated PMN usually underwent a time-dependent aging process and > 80% of PMN cultured in medium alone for 72 h showed morphologic features of PCD as depicted by hematoxylin and eosin staining as well as by electron microscopy. During the PCD process, untreated PMN not only exhibited condensed nuclear structure and decrease in cell size, but also displayed DNA fragmentation. DNA fragmentation in PMN was prevented by IL-2. Prevention of PCD by IL-2 was associated with an increase in new RNA and protein synthesis in PMN, which may reflect cytokine induction, such as tumor necrosis factor, as we have recently shown. Thus, our data expands our current understanding of PMN in that they may be an active component of the immune system, with a longer life-span when activated than expected.

Mechanism of Stimulatory Action of Growth Hormone on Ovarian Steroidogenesis in Spotted Seatrout, Cynoscion nebulosus

The mechanism of growth hormone's (bovine growth hormone, bGH) stimulatory action on steroidogenesis was examined using ovarian tissue of spotted seatrout ( Cynoscion nebulosus) in an in vitro incubation system and compared to that of a gonadotropin (human chorionic gonadotropin, hCG). Testosterone and estradiol production by seatrout ovaries in vitro were stimulated even with low concentrations of bGH (50 ng/ml), and increasing concentrations demonstrated a concentration-dependent relationship similar to that observed with hCG. The steroidogenic responses to combined treatments with bGH and hCG approximately equaled the sum of the stimulatory effects of the two hormones, possibly indicating that bGH does not potentiate the action of gonadotropin. Cyanoketone treatment of vitellogenic follicles inhibited bGH-induced estradiol production, but the stimulatory effect of bGH on the conversion of exogenous testosterone to estradiol was not altered by cyanoketone, which suggests that GH stimulates aromatase activity in addition to an earlier step in the biosynthetic pathway for estradiol production. The stimulatory effects of bGH and hCG on aromatase activity were mimicked by forskolin and dibutyryl cAMP, both of which are known to raise the intracellular level of cAMP. These results suggest that bGH as well as hCG-induced increases in aromatase activity are mediated through adenylate cyclase-cAMP-dependent mechanism(s). The cAMP content of ovarian follicles was markedly increased within 15 min of bGH stimulation and was maximal at 1 hr, whereas steroid production did not increase significantly until 30 min and was maximal after 3 to 9 hr of incubation. The cAMP response to bGH, like that of steroid production, was concentration-dependent. The time-course and concentration-response effects of bGH on cAMP accumulation and steroid production were similar to those of hCG and forskolin, although the magnitude of the responses was less. The addition of cycloheximide or actinomycin D to the media did not affect the basal production of estradiol but completely blocked the bGH and hCG stimulation of the aromatization of exogenous testosterone to estradiol. These results suggest that the stimulatory effects of bGH and hCG on aromatase activity depend upon the synthesis of new RNA and regulatory protein(s).

Cooperative Effects of Ciliary Neurotrophic Factor and Norepinephrine on Tyrosine Hydroxylase Expression in Cultured Rat Locus Coeruleus Neurons

Ciliary neurotrophic factor (CNTF) was found to promote the expression of tyrosine hydroxylase (TH) immunoreactivity by cultured noradrenergic neurons from the locus coeruleus (LC) of E18 rat fetuses, but only in the concomitant presence of norepinephrine (NE), their own neurotransmitter. The number of TH-positive cells in LC cultures was shown to decrease by 65% within 3 days and by 75% after 6 days. Treatment with 10 TU/ml human recombinant CNTF together with 1 μ M NE was able to fully maintain the initial number of TH-positive neurons for 3 days. This effect, however, was no longer seen after 6 days of continuous exposure. A 24-hr treatment with CNTF/NE was capable of completely restoring the initial number of TH-positive cells, even if its addition was delayed for 2 days. Moreover, when its addition was delayed for 5 days, CNTF/NE restored ∼80% of the TH-positive neurons that were initially present. These results suggest that the disappearance of TH-positive neurons in LC cultures is not due to their death, but rather to the reduced expression of TH and that the simultaneous exposure to CNTF and NE upregulates TH. Effects on TH-positive cell number were not evoked by CNTF or NE alone. The CNTF/NE effect was dependent on protein synthesis, but was only partially inhibited by RNA synthesis inhibitors, suggesting that both transcription from preexisting mRNA and synthesis of new RNA were stimulated. The effect of CNTF/NE was mediated by α 2-adrenoceptors, since it was blocked by α 2-antagonists and since α 2-agonists were able to substitute for NE. Our results suggest a novel mechanism of regulation of the phenotype of the noradrenergic LC neuron, involving the collaborative influences of CNTF and norepinephrine, their own neurotransmitter.

Action of Aldosterone on Cultured Renal Collecting Duct Cells during the Latent Period

The effects of aldosterone on protein synthesis in the latent period were investigated on cultured renal collecting duct cells from neonatal rabbit kidneys. Tissue was incubated with radioactively labelled uridine and amino acids and then precipitated with trichloroacetic acid in order to determine the intracellular precursor pool and identify new synthesis of RNA and protein. During the latent period, aldosterone increased the intracellular radioactive uridine pool and total radioactive RNA content already 20 and 60 min after its application; conversely 40 min after aldosterone introduction, no stimulation was found. Further experiments revealed that the intracellular radioactive amino acid pool was generally increased by aldosterone after 20, 40 and 60 min, while a distinct increased radioactive protein content was found to be induced by aldosterone only after 40 min. This indicates that aldosterone increases the uptake of RNA and protein precursors and the new synthesis of RNA and proteins. These events seem to to be regulated not continuously but intermittently. The induced proteins possibly take part in the mediation of the early hormone response. Experiments with the aldosterone antagonist, spironolactone, provide evidence for the specificity of the described hormone effects. The results after application of the Na+ channel blocker, amiloride, and the Na+/K(+)-ATPase inhibitor, G-strophanthin, indicate that the aldosterone effects are controlled by Na+ channels and Na+ pumps and therefore by the intracellular Na+ content. The inhibitory effect of cycloheximide on the aldosterone-induced protein synthesis indicates the role of these proteins on the hormone-stimulated Na+ transport.

Effects of steroids on the synthesis and metabolism of phosphataidylethanol in phorbol ester-activated lymphocytes

The phorbol ester 12-O-tetradecanoylphorbol-13-acetate activates the phospholipase D pathway in bovine lymphocytes, leading to a synthesis of phosphatidylethanol (PEt) from exogenous alcohol. Concomitant treatment of the cells with 10(-8) M etiocholanolone, dehydroepiandrosterone or 16 alpha-bromo-epiandrosterone results in the production of phosphatidylethanols that carry metabolically altered forms of arachidonic acid at position 2. The observed steroid response appears to be mediated by a receptor mechanism in that it depends on the synthesis of new RNA and protein. The spectrum of steroids producing the response suggests that the postulated receptor system may be distinct from the well-studied glucocorticoid, progesterone, estrogen and androgen specific receptors. The possible relevance of these new metabolites of ethanol to the problem of alcoholism in humans and to the field of carcinogenesis in general is discussed.

Increased prolyl hydroxylase activity and collagen synthesis in hepatocyte cultures exposed to superoxide.

Primary monolayer cultures of rat hepatocytes at confluence were exposed to an exogenously added source of superoxide, and its influence on collagen synthesis was examined. Superoxide was generated by the addition of dihydroxyfumarate to the culture medium. Exposure of hepatocytes to dihydroxyfumarate greatly stimulated the activity of prolyl hydroxylase and the synthesis of collagen. A significant increase in prolyl hydroxylase activity was observed with 5 micrograms per ml dihydroxyfumarate in 24 hr relative to that in the untreated cultures. Maximum stimulation of greater than 3-fold compared to the control value was elicited by 25 micrograms per ml dihydroxyfumarate. When scavengers of superoxide such as superoxide dismutase and Cu(Lys)2 were added in the medium, the increase in prolyl hydroxylase activity induced by dihydroxyfumarate was nearly abolished. Experiments with actinomycin D indicated that synthesis of new RNA was involved in the stimulation of prolyl hydroxylase activity. Analysis of collagen synthesis in cultures exposed to dihydroxyfumarate also showed a marked increase compared to that of the untreated cultures. The presence of superoxide dismutase in the medium significantly reduced the increase in collagen synthesis. Our results indicate that superoxide mediates the stimulation of collagen synthesis in hepatocytes. These findings may provide a possible explanation for excess collagen formation during induced liver fibrosis.

The regulated expression of Epstein-Barr virus: evidence that the transition from primary to secondary protein synthesis in Raji cells superinfected with Epstein-Barr virus requires the synthesis of new RNA.

In the presence of canavanine and the absence of arginine, superinfected Raji cells synthesize a limited spectrum of proteins (primary proteins). After the removal of canavanine at 8 h post infection, the cells proceed after a lag phase of 2-3 h to synthesize a second group of proteins. The appearance of these proteins can be prevented by addition of actinomycin-D to the chase media, suggesting that active primary proteins are required for the synthesis of new mRNA coding for the secondary proteins.

Depletion-replenishment of the testicular estrogen receptor: Sensitivity to cycloheximide and actinomycin D

Male rats (30–35 days old) were utilized to examine the process of depletion and replenishment of the testicular cytosolic estrogen receptor and to investigate the effects of cycloheximide and actinomycin D on these processes. The dose dependence and temporal nature of receptor depletion and replenishment were investigated. Maximum depletion (> 90%) occurred by 1 h after in vivo administration of either 5 or 10 μg estradiol-17β. Depletion of the cytosolic receptor at 1 h occurred concomitant to a marked increase in nuclear receptor thus indicating translocation. Receptor replenishment to control levels was observed by 6 h post treatment. To determine the requirements for transcriptional and translational events in the replenishment process, actinomycin D and cycloheximide were administered in vivo. Simultaneous treatment with cycloheximide and estradiol resulted in a significant inhibition of replenishment at 6 and 12 h post treatment of 46 and 60% below control levels, respectively. Cycloheximide treatment alone had no effect on receptor levels. A significant inhibition of replenishment at 6 h was also shown when cycloheximide was given 3 h after estradiol treatment. Cycloheximide administration at 6 h after estradiol significantly suppressed receptor levels at 12 h suggesting that replenished receptor levels at 6–12 h are in a state of rapid turnover. Receptor replenishment exhibited a different response to actinomycin D treatment in that significant inhibition was observed only when the drug was administered at 3 h after estradiol treatment. These results demonstrate that testicular cytosolic estrogen receptor depletion is dose and time dependent. The results further demonstrate that receptor replenishment involves protein synthesis and suggests that synthesis of new RNA might also be required.

Re-utilization of pyrimidine nucleotides during rat liver regeneration

The changes in the specific radioactivities of the pool of total acid-soluble uridine nucleotides and of uridine and cytidine components of total cellular and nuclear RNA were monitored in regenerating rat liver for 12 days after partial hepatectomy. Evidence is presented for the re-utilization of pyrimidine nucleotides derived from cytoplasmic RNA degradation for the synthesis of new RNA. The extent of recycling was assessed and the true rate of rRNA turnover determined more accurately. The reutilization of the uridine components of RNA was 7.0%/day during the proliferative and 3.2%/day during the post-proliferative phase, whereas that of the cytidine nucleotides was more pronounced (9.6%/day and 18.1%/day respectively). The results reveal the existence of partial compartmentalization of pyrimidine ribonucleoside triphosphate pools in the nucleus and cytoplasm of rat liver cells.

Ultrastructural localization of protein kinase subunits in glucagon-treated rat hepatocytes applying the colloidal-gold technique

The molecular mechanisms by which non-steroidal hormones regulate transcription in eukaryotes has not been elucidated. However, cyclic AMP, an important second messenger of the hormonal signal has been suggested to play a significant role in the regulation of eukaryotic gene expression (1). It has also been proposed that hormones functioning through the cAMP/adenylate cyclase system initiate a series of biochemical events in the target tissue resulting in the synthesis of new RNA and protein (2). The important link in this scheme appears to be the cAMP dependent protein kinase which may translocate from cytoplasm to nucleus following its activation by cAMP. Two types of soluble cAMP dependent protein kinases exist in mammalian tissues (type I and II). Each isozyme exists as a tetramer composed of two catalytic (C) and two regulatory (R) subunits. Binding of cAMP to the R subunit activates the C subunit according to the following stoichiometry: R2C2 + 4cAMP = R2·cAMP4 + 2C.

Macromolecular syntheses during the quick-change act of Naegleria.

The rapid, synchronous differentiation of N. gruberi from amoebae to flagellates is a useful paradigm to study aspects of cell differentiation, including regulation of the synthesis of proteins that are related to the changes in cell shape and motility, which occur during differentiation. The differentiation requires synthesis of new RNA and protein molecules to accomplish defined morphogenetic events. Specific new proteins, including the tubulins that form the flagellar microtubules, are synthesized at various times during differentiation, and particular mRNA species appear and disappear. The time course of the synthesis of the alpha and beta subunits of flagellar tubulin is paralleled by the programmed appearance and disappearance of flagellar tubulin mRNAs. The evidence supports the hypothesis that the synthesis of flagellar tubulin is regulated by the transcription, and subsequent disappearance, of flagellar tubulin mRNA. Translatable mRNAs for two calmodulin-like calcium-binding proteins appear and disappear contemporaneously with those for flagellar tubulin. During differentiation the synthesis of actin, the major protein of amoebae, is selectively shut down, and translatable actin mRNA rapidly disappears. This description of the orderly appearance, utilization, and disappearance of the mRNAs for actin, calcium-binding proteins, and flagellar tubulin during differentiation provides means and motivation to investigate the mechanisms that regulate these events.

Inhibition of chitin biosynthesis in cultured imaginal discs: Effects of alpha-amanitin, actinomycin-D, cycloheximide, and puromycin.

Wing imaginal discs isolated from last instar larvae of the Indian meal moth,Plodia interpunctella, produced chitin when incubated in vitro with ≧2×10-7 M 20-hydroxyecdysone. Chitin biosynthesis was initiated 8 h after the conclusion of a 24-h treatment with hormone. Simulataneous incubation of wing discs with 20-hydroxyecdysone and either inhibitors of RNA synthesis (alpha-amanitin, actinomycin-D) or inhibitors of protein systhesis (cycloheximide, puromycin) prevented chitin biosynthesis. We conclude from our results that RNA and protein synthesis must continue undiminished during the hormone-contact period, and that synthesis of protein, but not of new RNA is required during the posthormone culture period. Our findings are consistent with the hypothesis that ecdysteroids stimulate insect metamorphosis by promoting the synthesis of new RNA and protein during a hormone-dependent phase followed by hormone-independent protein synthesis.

Periodic, metabolic and structural phenomena in a protist, Euglena gracilis

Sychronous divisions of Euglena gracilis strain Z can be obtained by various methods. When the cells are cultivated in a medium containing lactate as the sole carbon source, synchronous divisions are observed, independent of the conditions of illumination. Nevertheless, there exists a relationship between the phase of cell division and ther periods of light and darkness applied to the culture. During the cell cycle, the synthesis of macromolecules is discontinuous--this is true of nuclear and mitochondrial DNA, ribosomal and nonribosomal RNA, and certain proteins (cytochrome c 558). Cyclic variations in the structure of mitochondria and chloroplasts are observed. In the course of the cell cycle, sequential metabolic processes accompany structural modifications of the organelles. Also, at the beginning of the cycle, at the start of phase G1, the cytoplasmic ribosomes are synthesized, and then, in green euglenids, nonribosomal RNAs are formed. These syntheses of RNA precede enlargement of the chondriome and plastids. In mid-G1 phase, a new synthesis of RNA begins, which precedes synthesis of nuclear and mitochondrial DNA. At the end of G1 phase, division of organelles starts, beginning with the chondriome and plastids, arranged in a network.

The maturation of rabbit epididymal spermatozoa in organ culture: inhibition by antiandrogens and inhibitors of ribonucleic acid and protein synthesis.

Infertile spermatozoa from the proximal corpus epididymidis will become fertile when this epididymal segment is cultured 24 h in vitro with 5alpha-dihydrotestosterone (5alpha-DHT). The effect of antiandrogens and inhibitors of RNA and protein synthesis upon this 5alpha-DHT-induced sperm maturation was investigated. The response to 5alpha-DHT was abolished by cyproterone acetate, SKF 7690, actinomycin D, cycloheximide, puromycin, and the aminonucleoside analog of puromycin. Addition of cyproterone acetate or actinomycin D to a suspension of distal corpus spermatozoa did not change their fertilizing ability. Culture of segments of the distal corpus for 24 h with the same antiandrogens and RNA and protein synthesis inhibitors did not change the fertilizing ability of spermatozoa. These results indicate that the development of the sperm-fertilizing ability observed in the proximal corpus epididymidis in vitro in response to 5alpha-DHT is dependent upon binding of 5alpha-DHT and synthesis of new RNA and protein molecules by the target cell. They also indicate that antiandrogen and inhibitors of RNA and protein synthesis do not have a nonspecific toxic effect on spermatozoa during the time period studied. It is likely that the target cells are the epididymal epithelial cells rather than the spermatozoa themselves.

A POSSIBLE MOLECULAR BASIS FOR OBLIGATE HOST‐PATHOGEN INTERACTIONS

SUMMARY This article is concerned with the molecular basis of host‐obligate‐parasite interactions that lead to either resistance or susceptibility of the host plants to obligate fungal pathogens. A scheme of molecular events that may occur during the primary stages of host‐pathogen interactions is proposed. It implies derepression of novel genes, intercistronic complementation of oligomeric enzymes in the host and the pathogen and, in some cases, complementation between host‐specific and pathogen‐specific polypeptides leading to the formation of catalytically different enzymes whose functions are essential for the continuation of the host‐parasite relationship. The basic tenets of the scheme are (a) transfer of nucleic acids, (b) synthesis of new RNA and proteins, (c) subunit interactions and formation of hybrid enzymes and (d) enzyme complementation during host‐parasite interactions. These are discussed in the light of some recent discoveries in plant pathology, biochemistry, virology and molecular biology. Transfer of macromolecules from one organism to another at the levels of (i) DNA, (ii) RNA or (iii) polypeptides frequently occurs in nature. Transfer of polypeptides (or amplified DNA segments or mRNA molecules coding for them) from pathogen to the host cells could lead to complementation between host‐specific and pathogen‐specific subunits of oligomeric enzymes. There are readily detectable changes in the transcription pattern at early stages of rust infection. Further analyses have shown that the observed changes in the pattern of gene expression are due to biochemically detectable alterations in the transcriptive specificity of RNA polymerases as well as in the template activity of chromatin. These findings are consistent with the derepression of novel genes in the host elicited by host‐pathogen interactions. Host‐pathogen interactions lead to the appearance of RNases with unique physical and catalytic properties. The appearance of these RNases coincides with (i) a remarkable increase in the rate of synthesis of all major classes of RNA molecules and (ii) an accumulation of RNA in the inoculated host suggesting an essential role of the new RNases in the post‐transcriptional processing of precursor RNA molecules.According to the postulated scheme, changes in the pattern of transcription and post‐transcriptional processing are brought about by intragenic and intergenic complementation of the enzymes involved in these processes including RNA poly‐merase and RNase molecules. The phenomenon of intragenic complementation has been observed in a large number of organisms including plants and fungi. In addition, fully functional hybrids of oligomeric enzymes have been produced in vitro with subunits from different tissues, species, genera, families and even phyla. In procaryotic systems, interactions of host‐specific and phage‐specific subunits leading to the formation of new enzymes are of common occurrence. In all oligomeric enzymes, relatively subtle changes in the subunit structure lead to radical changes in their catalytic and regulatory properties. This phenomenon is illustrated by the two enzyme systems, RNA polymerases and RNases. The mode of operation of the complementation model and its relevance to the host‐specificity of the pathogens and resistance or susceptibility of the host plants are described.