An effect of light on the production of ethylene and the growth of the plumular portion of etiolated pea seedlings

The production of ethylene by etiolated pea epicotyls (Pisum sativum L., cv. Alaska) is confined to the plumule and plumular hook portion of the epicotyl, and occurs at a rate of about 6 μl·kg⁻¹·hr⁻¹. Such a rate is sufficient to give physiologically active concentrations of ethylene within the tissue. Exposure of etiolated seedlings to a single dose of red light caused a transient decrease in ethylene production and a corresponding increase in plumular expansion. Far-red irradiation following the red light treatment decreased the red effect to the level achieved by the far-red alone, suggesting that the ethylene production mechanism is controlled by phytochrome and thus that the ethylene intervenes as a regulator in the phytochrome control of plumular expansion.     

Rice phytochrome A controls apical hook opening after a single light pulse in transgenic tobacco seedlings

Apical hook opening in tobacco seedlings can be induced by a single red light pulse and this induction can be reverted by a subsequent far-red light pulse. The slow hook opening kinetics and the reversibility of an inductive light pulse even after 8 h of darkness indicate the involvement of stable phytochrome. Compared with wild-type, transgenic BN1 seedlings which overexpress rice phytochrome A exhibit a higher sensitivity to low irradiance red light pulses. Moreover, in BN1 seedlings an inductive red light pulse is only partially reversible even after 30 min, whereas wild-type tobacco seedlings show complete reversibility during the entire hook opening process. The data found show that rice phytochrome A is active in transgenic tobacco seedlings in controlling hook opening and that the introduced rice phytochrome A and the endogenous stable phytochrome behave differently in this response.     

The Sphingolipid Receptor S1PR2 Is a Receptor for Nogo-A Repressing Synaptic Plasticity

Nogo-A is a membrane protein of the central nervous system (CNS) restricting neurite growth and synaptic plasticity via two extracellular domains: Nogo-66 and Nogo-A-Δ20. Receptors transducing Nogo-A-Δ20 signaling remained elusive so far. Here we identify the G protein-coupled receptor (GPCR) sphingosine 1-phosphate receptor 2 (S1PR2) as a Nogo-A-Δ20-specific receptor. Nogo-A-Δ20 binds S1PR2 on sites distinct from the pocket of the sphingolipid sphingosine 1-phosphate (S1P) and signals via the G protein G₁₃, the Rho GEF LARG, and RhoA. Deleting or blocking S1PR2 counteracts Nogo-A-Δ20- and myelin-mediated inhibition of neurite outgrowth and cell spreading. Blockade of S1PR2 strongly enhances long-term potentiation (LTP) in the hippocampus of wild-type but not Nogo-A^−/− mice, indicating a repressor function of the Nogo-A/S1PR2 axis in synaptic plasticity. A similar increase in LTP was also observed in the motor cortex after S1PR2 blockade. We propose a novel signaling model in which a GPCR functions as a receptor for two structurally unrelated ligands, a membrane protein and a sphingolipid. Elucidating Nogo-A/S1PR2 signaling platforms will provide new insights into regulation of synaptic plasticity.     

A diffusion model for mesoderm induction in amphibian embryos

In this paper we try to answer the question whether diffusion is a possible mechanism to explain mesoderm induction in Amphibians. First the embryological data are discussed and a hypothesis for mesoderm formation is set forth. The blastula being essentially a hollow sphere, we assume that the induction mechanism in an embryo at the blastula stage can be simulated by diffusion-reaction processes on spherical surfaces. A model is constructed for the simple case when the source is held constant with respect to time, the decay proportional to the concentration and the diffusion coefficient a constant, From simulation we find a (best) value for the decay constant to be 6 × 10^–5/sec and for the diffusion constant to be 0.24 × 10^{– 6} cm²/sec. The relation between the parameters is derived from an analytic solution for the diffusion process on a spherical surface with a continuously producing point source and the concentration proportional to the decay. The form and regulative properties of the steady concentration gradient are discussed.     

Photo-Induction and Automated Quantification of Reversible Mitochondrial Permeability Transition Pore Opening in Primary Mouse Myotubes

Opening of the mitochondrial permeability transition pore (mPTP) is involved in various cellular processes including apoptosis induction. Two distinct states of mPTP opening have been identified allowing the transfer of molecules with a molecular weight <1500 Da or <300 Da. The latter state is considered to be reversible and suggested to play a role in normal cell physiology. Here we present a strategy combining live-cell imaging and computer-assisted image processing allowing spatial visualization and quantitative analysis of reversible mPTP openings (“ΔΨ flickering”) in primary mouse myotubes. The latter were stained with the photosensitive cation TMRM, which partitions between the cytosol and mitochondrial matrix as a function of mitochondrial membrane potential (ΔΨ). Controlled illumination of TMRM-stained primary mouse myotubes induced ΔΨ flickering in particular parts of the cell (“flickering domains”). A novel quantitative automated analysis was developed and validated to detect and quantify the frequency, size, and location of individual ΔΨ flickering events in myotubes.     

Distribution and nonphotochemical transformation of phytochrome in subcellular fractions from pisum epicotyls

In etiolated pea (Pisum sativum L. cv. Alaska) shoots about 3% of the total extractable phytochrome was found in the mitochondrial fraction and about 4.5% in the microsomal fraction, while over 70% was soluble in the 105,000g supernatant. The value of Δ(ΔA) per milligram of protein was significantly higher in the 105,000g supernatant than in these particulate fractions. The percentage conversion of Pr to Pfr was approximately proportional to the total dose of red light in every subcellular fraction tested, unless the dose approached a saturation level. After a brief irradiation of intact shoots with red light at 26 C, each subcellular fraction showed different patterns of dark transformation in vivo at 26 C; that is, the amount of the particulate-bound phytochrome increased immediately after the irradiation, and a reversion of Pfr to Pr was indicated for the first 2 hr in the 12,000g supernatant, but not at all in the mitochondrial and microsomal fractions. The amounts of Pr in the mitochondrial and microsomal fractions did not change during the dark incubation, while those in the 12,000g supernatant increased with time. Similar results were obtained with apical shoot segments after exposure to red light at 0 C and a subsequent dark incubation on moist filter paper at 26 C.     

The role of uncoupling protein 2 in macrophages and its impact on obesity-induced adipose tissue inflammation and insulin resistance

The development of a chronic, low-grade inflammation originating from adipose tissue in obese subjects is widely recognized to induce insulin resistance, leading to the development of type 2 diabetes. The adipose tissue microenvironment drives specific metabolic reprogramming of adipose tissue macrophages, contributing to the induction of tissue inflammation. Uncoupling protein 2 (UCP2), a mitochondrial anion carrier, is thought to separately modulate inflammatory and metabolic processes in macrophages and is up-regulated in macrophages in the context of obesity and diabetes. Here, we investigate the role of UCP2 in macrophage activation in the context of obesity-induced adipose tissue inflammation and insulin resistance. Using a myeloid-specific knockout of UCP2 (Ucp2^ΔLysM), we found that UCP2 deficiency significantly increases glycolysis and oxidative respiration, both unstimulated and after inflammatory conditions. Strikingly, fatty acid loading abolished the metabolic differences between Ucp2^ΔLysM macrophages and their floxed controls. Furthermore, Ucp2^ΔLysM macrophages show attenuated pro-inflammatory responses toward Toll-like receptor-2 and -4 stimulation. To test the relevance of macrophage-specific Ucp2 deletion in vivo, Ucp2^ΔLysM and Ucp2^fl/fl mice were rendered obese and insulin resistant through high-fat feeding. Although no differences in adipose tissue inflammation or insulin resistance was found between the two genotypes, adipose tissue macrophages isolated from diet-induced obese Ucp2^ΔLysM mice showed decreased TNFα secretion after ex vivo lipopolysaccharide stimulation compared with their Ucp2^fl/fl littermates. Together, these results demonstrate that although UCP2 regulates both metabolism and the inflammatory response of macrophages, its activity is not crucial in shaping macrophage activation in the adipose tissue during obesity-induced insulin resistance.     

Failure of lactoperoxidase to iodinate specifically the plasma membrane of cucurbita tissue segments

An attempt has been made to use lactoperoxidase-catalyzed iodination of excised Cucurbita hypocotyl hooks to monitor the distribution of plasma membrane fragments relative to that of phytochrome in particulate fractions from this tissue. Upon fractionation, the iodinated tissue yields a 20,000g pellet which contains 58% of the trichloroacetic acid-precipitable ¹²⁵I at a specific radioactivity 12 times that of the proteins in the supernatant. On sucrose gradients, the labeled fraction has a mean isopycnic density of 1.15 g · cm⁻³. The distribution profile is distinct from that of the total particulate protein and does not coincide with either mitochondrial or endoplasmic reticulum markers. These observations satisfy operational criteria commonly accepted in other systems as indices of selective labeling of the cell surface. The sucrose gradient profiles of the phytochrome and ¹²⁵I in the 20,000g pellets are noncoincident. In the absence of more direct evidence, this is readily interpreted to indicate a lack of association of the pigment with the plasma membrane.     

A scale-down two-compartment reactor with controlled substrate oscillations: Metabolic response of Saccharomyces cerevisiae

Substrate concentration gradients are likely to appear during large scale fermentations. To study effects of such gradients on microorganisms, an aerated scale-down reactor system was constructed. It consists of a plug flow reactor (PFR) and a stirred tank reactor (STR), between which the medium is circulated. The PFR, which is an aerated static mixer reactor, was characterized with respect to plug flow behaviour and oxygen transfer. A Bodenstein number of 15–220, depending on residence time and aeration rate, and a k_La of 500–1130 h^–1, depending mainly on aeration rate, were obtained. The biological test system used, was aerobic ethanol production by Saccharomyces cerevisiae, due to sugar excess. The ethanol concentration profile and the yield of biomass were compared in two fed-batch fermentations. In the first case, the feeding point of molasses was located at the inlet of the PFR. This simulates location of the feeding point in the segregated part of a heterogeneous reactor, with local high sugar concentrations. In the second mode of operation, as a control with good mixing conditions, the PFR was disconnected from the STR, into which the substrate was fed. Differences were found: Up to 6% less biomass was produced and a larger amount of ethanol was formed in the two-compartment reactor system, due to the uneven sugar concentration distribution. This emphasizes the importance of the location of, and the mixing conditions at, the feeding point in a bioreactor.     

Cell Type–dependent Requirement for PIP Box–regulated Cdt1 Destruction During S Phase

DNA synthesis–coupled proteolysis of the prereplicative complex component Cdt1 by the CRL4^Cdt2 E3 ubiquitin ligase is thought to help prevent rereplication of the genome during S phase. To directly test whether CRL4^Cdt2-triggered destruction of Cdt1 is required for normal cell cycle progression in vivo, we expressed a mutant version of Drosophila Cdt1 (Dup), which lacks the PCNA-binding PIP box (Dup^ΔPIP) and which cannot be regulated by CRL4^Cdt2. Dup^ΔPIP is inappropriately stabilized during S phase and causes developmental defects when ectopically expressed. Dup^ΔPIP restores DNA synthesis to dup null mutant embryonic epidermal cells, but S phase is abnormal, and these cells do not progress into mitosis. In contrast, Dup^ΔPIP accumulation during S phase did not adversely affect progression through follicle cell endocycles in the ovary. In this tissue the combination of Dup^ΔPIP expression and a 50% reduction in Geminin gene dose resulted in egg chamber degeneration. We could not detect Dup hyperaccumulation using mutations in the CRL4^Cdt2 components Cul4 and Ddb1, likely because these cause pleiotropic effects that block cell proliferation. These data indicate that PIP box–mediated destruction of Dup is necessary for the cell division cycle and suggest that Geminin inhibition can restrain Dup^ΔPIP activity in some endocycling cell types.     

Intraspecific differences in metabolic rates shape carbon stable isotope trophic discrimination factors of muscle tissue in the common teleost Eurasian perch (Perca fluviatilis)

1. Stable isotopes represent a unique approach to provide insights into the ecology of organisms. δ¹³C and δ¹⁵N have specifically been used to obtain information on the trophic ecology and food‐web interactions. Trophic discrimination factors (TDF, Δ¹³C and Δ¹⁵N) describe the isotopic fractionation occurring from diet to consumer tissue, and these factors are critical for obtaining precise estimates within any application of δ¹³C and δ¹⁵N values. It is widely acknowledged that metabolism influences TDF, being responsible for different TDF between tissues of variable metabolic activity (e.g., liver vs. muscle tissue) or species body size (small vs. large). However, the connection between the variation of metabolism occurring within a single species during its ontogeny and TDF has rarely been considered.
2. Here, we conducted a 9‐month feeding experiment to report Δ¹³C and Δ¹⁵N of muscle and liver tissues for several weight classes of Eurasian perch (Perca fluviatilis), a widespread teleost often studied using stable isotopes, but without established TDF for feeding on a natural diet. In addition, we assessed the relationship between the standard metabolic rate (SMR) and TDF by measuring the oxygen consumption of the individuals.
3. Our results showed a significant negative relationship of SMR with Δ¹³C, and a significant positive relationship of SMR with Δ¹⁵N of muscle tissue, but not with TDF of liver tissue. SMR varies inversely with size, which translated into a significantly different TDF of muscle tissue between size classes.
4. In summary, our results emphasize the role of metabolism in shaping‐specific TDF (i.e., Δ¹³C and Δ¹⁵N of muscle tissue) and especially highlight the substantial differences between individuals of different ontogenetic stages within a species. Our findings thus have direct implications for the use of stable isotope data and the applications of stable isotopes in food‐web studies.

     

Zinc-Dependent Interaction between JAB1 and Pre-S2 Mutant Large Surface Antigen of Hepatitis B Virus and Its Implications for Viral Hepatocarcinogenesis

Chronic hepatitis B virus (HBV) infection is a major cause of hepatocellular carcinoma (HCC) worldwide. The pre-S₂ mutant large HBV surface protein (Δ2 LHBS), which contains an in-frame deletion of approximately 17 amino acids in LHBS, is highly associated with risks and prognoses of HBV-induced HCC. It was previously reported that Δ2 LHBS interacts with the Jun activation domain-binding protein 1 (JAB1), a zinc metalloprotease. This promotes the degradation of the cell cycle regulator p27^Kip1 and is believed to be the major mechanism for Δ2 LHBS-induced HCC. In this study, it was found that the interaction between JAB1 and Δ2 LHBS is facilitated by divalent metal Zn²⁺ ions. The binding of JAB1 to Δ2 LHBS requires the JAB1/CSN5 MPN metalloenzyme (JAMM) motif and residue H138 that binds to Zn²⁺ ions in JAB1. Isothermal titration calorimetry showed that Δ2 LHBS binds directly to Zn²⁺ ions in a two-site binding mode. Residues H71 and H116 in Δ2 LHBS, which also contact Zn²⁺ ions, are also indispensable for Δ2 LHBS-mediated p27^Kip1 degradation in human HuH7 cells. These results suggest that developing drugs that interrupt interactions between Δ2 LHBS and JAB1 can be used to mitigate Δ2 LHBS-associated risks for HCC.     

Urea perturbation and the reversibility of nucleohistone conformation

Urea effect on conformation and thermal stabilities in nucleohistone and NaCl-treated partially dehistonized nucleohistones has been studied by circular dichroism (CD) and thermal denaturation. Urea imposes a CD change at 278mm of DNA base pairs in native and NaCl-treated nucleohistones which can be decomposed into two parts: a decrease in Δε₂₇₈ for histone-free base pairs and an increase for histone-bound base pairs. The reduction by urea of Δε₂₂₀ of bound histones is approximately proportional to the increase of Δε₂₇₈ of histone-bound base pairs. Urea also lowers the melting temperatures of base pairs both free and bound by histones. The presence of urea indeed destroys the secondary structure of bound histones, causing changes in the conformation and thermal stabilities of histone-bound base pairs in nucleohistone. Such a urea perturbation on nucleohistone conformation is reversible.     

Natural Isotopic Signatures of Variations in Body Nitrogen Fluxes: A Compartmental Model Analysis

Body tissues are generally ¹⁵N-enriched over the diet, with a discrimination factor (Δ¹⁵N) that varies among tissues and individuals as a function of their nutritional and physiopathological condition. However, both ¹⁵N bioaccumulation and intra- and inter-individual Δ¹⁵N variations are still poorly understood, so that theoretical models are required to understand their underlying mechanisms. Using experimental Δ¹⁵N measurements in rats, we developed a multi-compartmental model that provides the first detailed representation of the complex functioning of the body''s Δ¹⁵N system, by explicitly linking the sizes and Δ¹⁵N values of 21 nitrogen pools to the rates and isotope effects of 49 nitrogen metabolic fluxes. We have shown that (i) besides urea production, several metabolic pathways (e.g., protein synthesis, amino acid intracellular metabolism, urea recycling and intestinal absorption or secretion) are most probably associated with isotope fractionation and together contribute to ¹⁵N accumulation in tissues, (ii) the Δ¹⁵N of a tissue at steady-state is not affected by variations of its P turnover rate, but can vary according to the relative orientation of tissue free amino acids towards oxidation vs. protein synthesis, (iii) at the whole-body level, Δ¹⁵N variations result from variations in the body partitioning of nitrogen fluxes (e.g., urea production, urea recycling and amino acid exchanges), with or without changes in nitrogen balance, (iv) any deviation from the optimal amino acid intake, in terms of both quality and quantity, causes a global rise in tissue Δ¹⁵N, and (v) Δ¹⁵N variations differ between tissues depending on the metabolic changes involved, which can therefore be identified using simultaneous multi-tissue Δ¹⁵N measurements. This work provides proof of concept that Δ¹⁵N measurements constitute a new promising tool to investigate how metabolic fluxes are nutritionally or physiopathologically reorganized or altered. The existence of such natural and interpretable isotopic biomarkers promises interesting applications in nutrition and health.     

Prolongation of MGE 412 Transposition Induction after γ-Irradiation in an Isogenic Line of Drosophila melanogaster

The dose dependence of the rate of -induced transpositions and consequent dynamics of the MGE 412pattern after -irradiation were investigated in isogenic line 49 in generations F₁, F₁₂, F₁₄₀, and F₁₇₀. It was shown that the results on dose dependence of transpositions was very similar with the corresponding results of the classic works by Timofeeff-Ressovsky et al.(1935). It is suggested that the transcribed copies of retrotransposon 412cure -radiation-induced double-strand DNA breaks. The phenomenon of prolongation of MGE transposition induction during early generations after treatment was shown. In this period (F₁–F₁₂), the maximum transposition rate ( 2 × 10^–2events per MGE copy, per haploid genome, per generation) and the maximum number of heterozygous MGE copies were achieved. In the late generations (F₁₄₀–F₁₇₀), the reduced induction level ( 10^–3) was established. In the population of effective size N _e= 2000 individuals, this corresponds to the state when 1/4N _e, i.e., when the transposition flow prevails over the MGE copy loss by genetic drift. These data together with some indirect evidence argue for the hypothesis that the spontaneous transposition rate is proportional to the average number of heterozygous MGE copies per diploid genome.     

Proton motive force during growth of Streptococcus lactis cells

Experiments with the aerotolerant anaerobe Streptococcus lactis provide the opportunity for determining the proton motive force (Δp) in dividing cells. The two components of Δp, ΔΨ (the transmembrane potential) and ΔpH (the chemical gradient of H⁺), were determined by the accumulation of radiolabeled tetraphenylphosphonium (TPP⁺) and benzoate ions. The ΔΨ was calibrated with the K⁺ diffusion potential in starved, valinomycin-treated cells. With resting, glycolyzing cells, the Δp was measured also by the accumulation of the non-metabolizable sugar thiomethyl-β-galactoside (TMG). In resting cells the Δp, calculated either by adding ΔΨ and ZΔpH or from the levels of TMG, was relatively constant between pH 5 to 7, decreasing from 160 to 150 mV and decreasing further to 100 mV at pH 8.0. With the TPP⁺ probe for ΔΨ, we confirmed our previous finding that the K⁺ ions dissipate ΔΨ and increase ΔpH, whereas Na⁺ ions have little effect on ΔΨ and no effect on ΔpH. [³H]TPP⁺ and [¹⁴C]benzoate were added during exponential phase to S. lactis cells growing at pH 5 to 7 at 28°C in a defined medium with glucose as energy source. As with resting cells, the ΔpH and ΔΨ were dependent on the pH of the medium. At pH 5.1, the ΔpH was equivalent to 60 mV (alkaline inside) and decreased to 25 mV at pH 6.8. The ΔΨ increased from 83 mV (negative inside) at pH 5.1 to 108 mV at pH 6.8. The Δp, therefore, was fairly constant between pH 5 and 7, decreasing from 143 to 133 mV. The values for Δp in growing cells, just as in resting cells, are consistent with a system in which the net efflux of H⁺ ions is effected by a membrane-bound adenosine triphosphatase and glycolytically generated adenosine triphosphate. The data suggest that in both growing and resting cells the pH of the medium and its K⁺ concentration are the two principal factors that determine the relative contribution of ΔpH and ΔΨ to the proton motive force.     

Effect of Pressure-Induced Changes in the Ionization Equilibria of Buffers on Inactivation of Escherichia coli and Staphylococcus aureus by High Hydrostatic Pressure

Survival rates of Escherichia coli and Staphylococcus aureus after high-pressure treatment in buffers that had large or small reaction volumes (ΔV°), and which therefore underwent large or small changes in pH under pressure, were compared. At a low buffer concentration of 0.005 M, survival was, as expected, better in MOPS (morpholinepropanesulfonic acid), HEPES, and Tris, whose ΔV° values are approximately 5.0 to 7.0 cm³ mol⁻¹, than in phosphate or dimethyl glutarate (DMG), whose ΔV° values are about −25 cm³ mol⁻¹. However, at a concentration of 0.1 M, survival was unexpectedly better in phosphate and DMG than in MOPS, HEPES, or Tris. This was because the baroprotective effect of phosphate and DMG increased much more rapidly with increasing concentration than it did with MOPS, HEPES, or Tris. Further comparisons of survival in solutions of salts expected to cause large electrostriction effects (Na₂SO₄ and CaCl₂) and those causing lower electrostriction (NaCl and KCl) were made. The salts with divalent ions were protective at much lower concentrations than salts with monovalent ions. Buffers and salts both protected against transient membrane disruption in E. coli, but the molar concentrations necessary for membrane protection were much lower for phosphate and Na₂SO₄ than for HEPES and NaCl. Possible protective mechanisms discussed include effects of electrolytes on water compressibility and kosmotropic and specific ion effects. The results of this systematic study will be of considerable practical significance in studies of pressure inactivation of microbes under defined conditions but also raise important fundamental questions regarding the mechanisms of baroprotection by ionic solutes.     

Effect of Delta-9-Tetrahydrocannabinol on Mouse Resistance to Systemic Candida albicans Infection

Delta-9-tetrahydrocannabinol (Δ⁹-THC), the psychoactive component of marijuana, is known to suppress the immune responses to bacterial, viral and protozoan infections, but its effects on fungal infections have not been studied. Therefore, we investigated the effects of chronic Δ⁹-THC treatment on mouse resistance to systemic Candida albicans (C. albicans) infection. To determine the outcome of chronic Δ⁹-THC treatment on primary, acute systemic candidiasis, c57BL/6 mice were given vehicle or Δ⁹-THC (16 mg/kg) in vehicle on days 1–4, 8–11 and 15–18. On day 19, mice were infected with 5×10⁵ C. albicans. We also determined the effect of chronic Δ⁹-THC (4–64 mg/kg) treatment on mice infected with a non-lethal dose of 7.5×10⁴ C. albicans on day 2, followed by a higher challenge with 5×10⁵ C. albicans on day 19. Mouse resistance to the infection was assessed by survival and tissue fungal load. Serum cytokine levels were determine to evaluate the immune responses. In the acute infection, chronic Δ⁹-THC treatment had no effect on mouse survival or tissue fungal load when compared to vehicle treated mice. However, Δ⁹-THC significantly suppressed IL-12p70 and IL-12p40 as well as marginally suppressed IL-17 versus vehicle treated mice. In comparison, when mice were given a secondary yeast infection, Δ⁹-THC significantly decreased survival, increased tissue fungal burden and suppressed serum IFN-γ and IL-12p40 levels compared to vehicle treated mice. The data showed that chronic Δ⁹-THC treatment decreased the efficacy of the memory immune response to candida infection, which correlated with a decrease in IFN-γ that was only observed after the secondary candida challenge.     

Effects of inhibitors of RNA and protein synthesis on bean hypocotyl hook opening and their implications regarding phytochrome action

Summary Inhibitors of protein and RNA synthesis (cycloheximide, puromycin, chloramphenicol, and actinomycin D), as well as Co⁺⁺, induce opening of the hypocotyl hook of bean seedlings during the early stage of the opening period both in the darkness and red light. The response is transitory, however, complete straightening of a hook can not be achieved in the presence of these agents. These agents abolish the response of hooks to red illumination. They also block the suppression of hook opening caused by IAA and ethylene. The response and sensitivity to GA are not affected by the inhibitors. Inhibitors of DNA synthesis (FUDR and mitomycin C) have no effect on hook opening. It appears that in this growth response RNA and protein synthesis are more immediately involved in ethylene action than they are in the cell elongation process or the action of GA thereon.The results indicate that phytochrome does not induce hook opening simply by activating genes whose products directly promote growth. It is suggested that the regulation of ethylene formation by light and auxins may be exerted by way of influences on tissue levels of phenolic inhibitors of ethylene biosynthesis.