Cat2 Mutants Research Articles

Characterization of the putative amino acid transporter genes AtCAT2, 3 &4: The tonoplast localized AtCAT2 regulates soluble leaf amino acids

The plant vacuole constitutes a large transient storage compartment for nutrients, proteins and metabolites, and is a major cellular sink for toxic waste compounds. Amino acids can cross the vacuolar membrane via specific transport proteins, which are molecularly not well characterized. Two members of a small subfamily of the cationic amino acid transporters, AtCAT2 and AtCAT4, were primarily localized at the tonoplast when tagged with GFP. The closely related AtCAT3, by contrast, was detected in the endoplasmic reticulum membrane. The exchange of a di-acidic motif at the carboxy-tail affected their sub-cellular localization, with larger effects visible in transiently transformed protoplasts compared to stably expressing plant lines. The genes have broad, partially overlapping tissue expression, with CAT2 dominating in most tissues. Loss-of-function mutants of individual CATs showed no visible phenotype under various conditions, but the overall tissue concentration of amino acids was increased in soil-grown cat2 mutants. The data suggest that CAT2 is a critical target of leaf amino acid concentrations and manipulation of this tonoplast transporter can significantly alter total tissue amino acid concentrations.

Activation of auxin signalling counteracts photorespiratory H2O2-dependent cell death.

The high metabolic flux through photorespiration constitutes a significant part of the carbon cycle. Although the major enzymatic steps of the photorespiratory pathway are well characterized, little information is available on the functional significance of photorespiration beyond carbon recycling. Particularly important in this respect is the peroxisomal catalase activity which removes photorespiratory H2O2 generated during the oxidation of glycolate to glyoxylate, thus maintaining the cellular redox homeostasis governing the perception, integration and execution of stress responses. By performing a chemical screen, we identified 34 small molecules that alleviate the negative effects of photorespiration in Arabidopsis thaliana mutants lacking photorespiratory catalase (cat2). The chlorophyll fluorescence parameter photosystem II maximum efficiency (Fv′/Fm′) was used as a high-throughput readout. The most potent chemical that could rescue the photorespiratory phenotype of cat2 is a pro-auxin that contains a synthetic auxin-like substructure belonging to the phenoxy herbicide family, which can be released in planta. The naturally occurring indole-3-acetic acid (IAA) and other chemically distinct synthetic auxins also inhibited the photorespiratory-dependent cell death in cat2 mutants, implying a role for auxin signalling in stress tolerance.

Highly Oxidized Peroxisomes Are Selectively Degraded via Autophagy in Arabidopsis

The positioning of peroxisomes in a cell is a regulated process that is closely associated with their functions. Using this feature of the peroxisomal positioning as a criterion, we identified three Arabidopsis thaliana mutants (peroxisome unusual positioning1 [peup1], peup2, and peup4) that contain aggregated peroxisomes. We found that the PEUP1, PEUP2, and PEUP4 were identical to Autophagy-related2 (ATG2), ATG18a, and ATG7, respectively, which are involved in the autophagic system. The number of peroxisomes was increased and the peroxisomal proteins were highly accumulated in the peup1 mutant, suggesting that peroxisome degradation by autophagy (pexophagy) is deficient in the peup1 mutant. These aggregated peroxisomes contained high levels of inactive catalase and were more oxidative than those of the wild type, indicating that peroxisome aggregates comprise damaged peroxisomes. In addition, peroxisome aggregation was induced in wild-type plants by exogenous application of hydrogen peroxide. The cat2 mutant also contained peroxisome aggregates. These findings demonstrate that hydrogen peroxide as a result of catalase inactivation is the inducer of peroxisome aggregation. Furthermore, an autophagosome marker, ATG8, frequently colocalized with peroxisome aggregates, indicating that peroxisomes damaged by hydrogen peroxide are selectively degraded by autophagy in the wild type. Our data provide evidence that autophagy is crucial for quality control mechanisms for peroxisomes in Arabidopsis.

Catalase andNO CATALASE ACTIVITY1Promote Autophagy-Dependent Cell Death inArabidopsis

Programmed cell death often depends on generation of reactive oxygen species, which can be detoxified by antioxidative enzymes, including catalases. We previously isolated catalase-deficient mutants (cat2) in a screen for resistance to hydroxyurea-induced cell death. Here, we identify an Arabidopsis thaliana hydroxyurea-resistant autophagy mutant, atg2, which also shows reduced sensitivity to cell death triggered by the bacterial effector avrRpm1. To test if catalase deficiency likewise affected both hydroxyurea and avrRpm1 sensitivity, we selected mutants with extremely low catalase activities and showed that they carried mutations in a gene that we named NO CATALASE ACTIVITY1 (NCA1). nca1 mutants showed severely reduced activities of all three catalase isoforms in Arabidopsis, and loss of NCA1 function led to strong suppression of RPM1-triggered cell death. Basal and starvation-induced autophagy appeared normal in the nca1 and cat2 mutants. By contrast, autophagic degradation induced by avrRpm1 challenge was compromised, indicating that catalase acted upstream of immunity-triggered autophagy. The direct interaction of catalase with reactive oxygen species could allow catalase to act as a molecular link between reactive oxygen species and the promotion of autophagy-dependent cell death.

Inhibition of gustatory plasticity due to acute nicotine exposure in the nematode Caenorhabditis elegans

The present study investigated the effect of nicotine exposure on gustatory plasticity in the nematode Caenorhabditis elegans. The chemotactic response of wild-type N2 nematodes pre-exposed to 100mM NaCl with 3.0mM nicotine was almost the same as that of mock-conditioned nematodes unexposed to NaCl; however, the response of N2 nematodes pre-exposed to NaCl without nicotine was significantly lower than that of mock-conditioned nematodes. These results indicate that gustatory plasticity is inhibited by acute nicotine exposure. Inhibition of gustatory plasticity was observed when cat-2 mutants with a defect in dopamine biosynthesis were pre-exposed to NaCl with 3.0mM nicotine. Acute nicotine exposure did not cause inhibition of gustatory plasticity in bas-1 mutants, which had defects in both serotonin and dopamine secretion, and tph-1 mutants, which had a defect in serotonin secretion only. However, inhibition of gustatory plasticity was observed when bas-1 and tph-1 mutants were maintained on a growth plate that included serotonin. These results suggest that serotonin signaling plays an essential role in the modulation of the acute effects of nicotine.

Defective root growth triggered by oxidative stress is controlled through the expression of cell cycle-related genes

Reactive oxygen species (ROS) have many functions in aerobic organisms. High levels of ROS can have a negative impact on plant cells leading to senescence and cell death. ROS accumulates in cells subjected to environmental stress and induces a cellular response to this external stimulus. To protect cells from the negative impacts of excess ROS, plants also possess a ROS detoxifying system to maintain normal ROS levels. The regulation of ROS levels is particularly important as ROS also functions as an important signal molecule and can regulate plant growth by modulating gene expression. Despite the functional importance of ROS signaling, little is known about the molecular mechanisms involved in the regulation of gene expression through ROS. Therefore, the present study investigated the effect of hydrogen peroxide (H2O2), a ROS compound, on cell cycle-related gene expression. Gene expression analyses coupled with microdissected sections of the developmental zone of Arabidopsis root tips revealed that H2O2 affects the expression of cell cycle-related genes. Additionally, ROS scavenging enzymes were found to play an important role in the root growth phenotype induced by H2O2. Specifically, root growth inhibition by H2O2 was diminished in transgenic Arabidopis overexpressing peroxidase but increased in a catalase2 (cat2) mutant. The strong root growth inhibition observed in the cat2 mutant upon H2O2 treatment indicated that CAT2 has an essential role in maintaining root meristem activity in the presence of oxidative stress. Overall, these results confirm that ROS function not only as stress-related compounds but that they also function as signaling molecules to regulate the progression of the cell cycle in root tips.

The Roles ofCATALASE2in Abscisic Acid Signaling inArabidopsisGuard Cells

We investigated the roles of catalase (CAT) in abscisic acid (ABA)-induced stomatal closure using a cat2 mutant and an inhibitor of CAT, 3-aminotriazole (AT). Constitutive reactive oxygen species (ROS) accumulation due to the CAT2 mutation and AT treatment did not affect stomatal aperture in the absence of ABA, whereas ABA-induced stomatal closure, ROS production, and [Ca(2+)](cyt) oscillation were enhanced.

Increased intracellular H2O2 availability preferentially drives glutathione accumulation in vacuoles and chloroplasts

One biochemical response to increased H₂O₂ availability is the accumulation of glutathione disulphide (GSSG), the disulphide form of the key redox buffer glutathione. It remains unclear how this potentially important oxidative stress response impacts on the different sub-cellular glutathione pools. We addressed this question by using two independent in situ glutathione labelling techniques in Arabidopsis wild type (Col-0) and the GSSG-accumulating cat2 mutant. A comparison of in situ labelling with monochlorobimane (MCB) and in vitro labelling with monobromobimane (MBB) revealed that, whereas in situ labelling of Col-0 leaf glutathione was complete within 2 h incubation, about 50% of leaf glutathione remained inaccessible to MCB in cat2. High-performance liquid chromatography (HPLC) and enzymatic assays showed that this correlated tightly with the glutathione redox state, pointing to significant in vivo pools of GSSG in cat2 that were unavailable for MCB labelling. Immunogold labelling of leaf sections to estimate sub-cellular glutathione distribution showed that the accumulated GSSG in cat2 was associated with only a minor increase in cytosolic glutathione but with a 3- and 10-fold increase in plastid and vacuolar pools, respectively. The data are used to estimate compartment-specific glutathione concentrations under optimal and oxidative stress conditions, and the implications for redox homeostasis and signalling are discussed.

Functional comparison of catalase genes in the elimination of photorespiratory H2O2 using promoter‐ and 3′‐untranslated region exchange experiments in the Arabidopsis cat2 photorespiratory mutant

Photorespiration-associated production of H(2) O(2) accounts for the majority of total H(2) O(2) in leaves of C(3) plants and is mainly eliminated by catalases. In Arabidopsis, lack of CAT2, but not CAT1 or CAT3, results in growth suppression and a marked accumulation of H(2) O(2) in leaves. To evaluate the contribution of individual catalase genes and their promoters to catalase function, we investigated the growth suppression and H(2) O(2) accumulation phenotypes of Arabidopsis derivatives expressing catalase genes from heterologous CAT promoters in a cat2 mutant background. The expression of CAT2 from the CAT2 promoter restored the wild-type phenotype in a cat2-1 mutant, while CAT1 and CAT3 promoter-driven expression of CAT2 did not. Ectopic expression of CAT3 from the CAT2 promoter also restored the normal phenotype, unlike that of CAT1 which required replacement of the CAT1 3'-untranslated region (UTR) with that of CAT2. These results demonstrated that the photorespiratory role of CAT2 is determined mainly by the regulation of its promoter activity. The 3'-UTR of CAT2 was vital for controlling CAT2 protein levels under photorespiratory conditions. Identification of component of heterotetramers catalase isoforms suggested that there is some functional redundancy between CAT2 and CAT1 and CAT3.

Enhancement of Chemotactic Response to Sodium Acetate in the NematodeCaenorhabditis elegans

In this study, we investigated the chemotactic response of a wild-type (N2) nematode (Caenorhabditis elegans) to a water-soluble attractant, sodium acetate, after pre-exposure to the chemical. The chemotactic response to 1.0 M sodium acetate of the non-exposed control nematodes was lower than that of the nematodes that were pre-exposed to 1.0 M sodium acetate for 90 min (p < 0.05). The increase in the response to sodium acetate was observed up to 6 hr, but not at 12 hr after exposure. To clarify the mechanism of this enhancement of the chemotactic response, several mutants were used. The chemotactic response of pre-exposed tph-1 and bas-1 mutants, whose main defect was serotonin secretion, was enhanced in comparison with that of the control mutants (p < 0.01). However, cat-1 and cat-2 mutants, which are respectively defective in serotonin and dopamine secretion and dopamine secretion only, showed no enhancement of the chemotactic response to sodium acetate, even when pre-exposed to this chemical. When the cat-1 and cat-2 mutants were pre-exposed to sodium acetate and bred in the presence of 40 mM dopamine, these mutants showed enhanced chemotactic response to sodium acetate (p < 0.05). These results suggest that the enhancement of chemotactic response to sodium acetate after pre-exposure to this chemical is modulated by dopaminergic neurotransmission.

The in Vivo Toxicity of Hydroxyurea Depends on Its Direct Target Catalase

Hydroxyurea (HU) is a well tolerated ribonucleotide reductase inhibitor effective in HIV, sickle cell disease, and blood cancer therapy. Despite a positive initial response, however, most treated cancers eventually progress due to development of HU resistance. Although RNR properties influence HU resistance in cell lines, the mechanisms underlying cancer HU resistance in vivo remain unclear. To address this issue, we screened for HU resistance in the plant Arabidopsis thaliana and identified seventeen unique catalase mutants, thereby establishing that HU toxicity depends on catalase in vivo. We further demonstrated that catalase is a direct HU target by showing that HU acts as a competitive inhibitor of catalase-mediated hydrogen peroxide decomposition. Considering also that catalase can accelerate HU decomposition in vitro and that co-treatment with another catalase inhibitor alleviates HU effects in vivo, our findings suggests that HU could act as a catalase-activated pro-drug. Clinically, we found high catalase activity in circulating cells from untreated chronic myeloid leukemia, offering a possible explanation for the efficacy of HU against this malignancy.

Peroxisomal Hydrogen Peroxide Is Coupled to Biotic Defense Responses by ISOCHORISMATE SYNTHASE1 in a Daylength-Related Manner

While it is well established that reactive oxygen species can induce cell death, intracellularly generated oxidative stress does not induce lesions in the Arabidopsis (Arabidopsis thaliana) photorespiratory mutant cat2 when plants are grown in short days (SD). One interpretation of this observation is that a function necessary to couple peroxisomal hydrogen peroxide (H(2)O(2))-triggered oxidative stress to cell death is only operative in long days (LD). Like lesion formation, pathogenesis-related genes and camalexin were only induced in cat2 in LD, despite less severe intracellular redox perturbation compared with SD. Lesion formation triggered by peroxisomal H(2)O(2) was modified by introducing secondary mutations into the cat2 background and was completely absent in cat2 sid2 double mutants, in which ISOCHORISMATE SYNTHASE1 (ICS1) activity is defective. In addition to H(2)O(2)-induced salicylic acid (SA) accumulation, the sid2 mutation in ICS1 abolished a range of LD-dependent pathogen responses in cat2, while supplementation of cat2 with SA in SD activated these responses. Nontargeted transcript and metabolite profiling identified clusters of genes and small molecules associated with the daylength-dependent ICS1-mediated relay of H(2)O(2) signaling. The effect of oxidative stress in cat2 on resistance to biotic challenge was dependent on both growth daylength and ICS1. We conclude that (1) lesions induced by intracellular oxidative stress originating in the peroxisomes can be genetically reverted; (2) the isochorismate pathway of SA synthesis couples intracellular oxidative stress to cell death and associated disease resistance responses; and (3) camalexin accumulation was strictly dependent on the simultaneous presence of both H(2)O(2) and SA signals.

The C. elegans D2-like dopamine receptor DOP-3 decreases behavioral sensitivity to the olfactory stimulus 1-octanol.

We previously found that dopamine signaling modulates the sensitivity of wild-type C. elegans to the aversive odorant 1-octanol. C. elegans lacking the CAT-2 tyrosine hydroxylase enzyme, which is required for dopamine biosynthesis, are hypersensitive in their behavioral avoidance of dilute concentrations of octanol. Dopamine can also modulate the context-dependent response of C. elegans lacking RGS-3 function, a negative regulator of Gα signaling. rgs-3 mutant animals are defective in their avoidance of 100% octanol when they are assayed in the absence of food (E. coli bacterial lawn), but their response is restored when they are assayed in the presence of food or exogenous dopamine. However, it is not known which receptor might be mediating dopamine's effects on octanol avoidance. Herein we describe a role for the C. elegans D2-like receptor DOP-3 in the regulation of olfactory sensitivity. We show that DOP-3 is required for the ability of food and exogenous dopamine to rescue the octanol avoidance defect of rgs-3 mutant animals. In addition, otherwise wild-type animals lacking DOP-3 function are hypersensitive to dilute octanol, reminiscent of cat-2 mutants. Furthermore, we demonstrate that DOP-3 function in the ASH sensory neurons is sufficient to rescue the hypersensitivity of dop-3 mutant animals, while dop-3 RNAi knockdown in ASH results in octanol hypersensitivity. Taken together, our data suggest that dopaminergic signaling through DOP-3 normally acts to dampen ASH signaling and behavioral sensitivity to octanol.

Arabidopsis thaliana Metallothionein, AtMT2a, Mediates ROS Balance during Oxidative Stress

Cold stress has been shown to induce the production of reactive oxygen species (ROS), which can elicit a potentially damaging oxidative burden on cellular metabolism. Here, the expression of a metallothionein gene (AtMT2a) was upregulated under low temperature and hydrogen peroxide (H2O2) stresses. The Arabidopsis T-DNA insertion mutant, mt2a, exhibited more sensitivity to cold stress compared to WT plants during the seed germination, and H2O2 levels in mt2a mutant were higher than that in WT plants during the cold stress. Synthetic GFP fused to AtMT2a was observed to be localized in cytosol. These results indicated that AtMT2a functions in tolerance against cold stress by mediating the ROS balance in the cytosol. Interestingly, mRNA level of AtMT2a was increased in seedlings of Arabidopsis cat2 mutant after cold treatment compared to WT seedlings, and overexpression of AtMT2a in cat2 could improve CAT activity under chilling stress. Moreover, the enzymatic activity of CAT in mt2a was higher than that in WT plants after cold treatment, suggesting that AtMT2a and CAT might complement each other in antioxidative process potentially in Arabidopsis. Taken together, our results provided a novel insight into the relationship between MTs and antioxidative enzymes in the ROS-scavenging system in plants.

Ethanol preference in C. elegans

Caenorhabditis elegans senses multiple environmental stimuli through sensory systems and rapidly changes its behaviors for survival. With a simple and well-characterized nervous system, C. elegans is a suitable animal model for studying behavioral plasticity. Previous studies have shown acute neurodepressive effects of ethanol on multiple behaviors of C. elegans similar to the effect of ethanol on other organisms. Caenorhabditis elegans also develops ethanol tolerance during continuous exposure to ethanol. In mammals, chronic ethanol exposure leads to ethanol tolerance as well as increased ethanol consumption. Ethanol preference is associated with the development of tolerance and may lead to the development of ethanol dependence. In this study, we show that C. elegans is a useful model organism for studying chronic effects of ethanol, including the development of ethanol preference. We designed a behavioral assay for testing ethanol preference after prolonged ethanol exposure. Despite baseline aversive responses to ethanol, animals show ethanol preference after 4 h of pre-exposure to ethanol and exhibit significantly enhanced preference for ethanol after a lifetime of ethanol exposure. The cat-2 and tph-1 mutant animals have defects in the synthetic enzymes for dopamine and serotonin, respectively. These mutants are deficient in the development of ethanol preference, indicating that dopamine and serotonin are required for this form of behavioral plasticity.

Bilobalide modulates serotonin-controlled behaviors in the nematode Caenorhabditis elegans

BackgroundDysfunctions in the serotonergic system have been implicated in several neurological disorders such as depression. Elderly individuals who have been diagnosed with clinical depression show elevated cases of neurodegenerative diseases. This has led to suggestions that modulating the serotonin (5-HT) system could provide an alternative method to current therapies for alleviating these pathologies. The neuroprotective effects of bilobalide in vitro have been documented. We aim to determine whether bilobalide affects the 5-HT system in the nematode C. elegans. The wild type worms, as well as well-characterized 5-HT mutants, were fed with bilobalide in a range of concentrations, and several 5-HT controlled behaviors were tested.ResultsWe observed that bilobalide significantly inhibited 5-HT-controlled egg-laying behavior in a dose-dependent manner, which was blocked in the 5-HT receptor mutants (ser-4, mod-1), but not in the 5-HT transporter (mod-5) or synthesis (tph-1) mutants. Bilobalide also potentiated a 5-HT-controlled, experience-dependent locomotory behavior, termed the enhanced slowing response in the wild type animals. However, this effect was fully blocked in 5-HT receptor mod-1 and dopamine defective cat-2 mutants, but only partially blocked in ser-4 mutants. We also demonstrated that acetylcholine transmission was inhibited in a transgenic C. elegans strain that constitutively expresses Aβ, and bilobalide did not significantly affect this inhibition.ConclusionThese results suggest that bilobalide may modulate specific 5-HT receptor subtypes, which involves interplay with dopamine transmission. Additional studies for the function of bilobalide in neurotransmitter systems could aid in our understanding of its neuroprotective properties.

Effects of Ionizing Radiation on Locomotory Behavior and Mechanosensation in Caenorhabditis elegans

Locomotory behavior (motility) and mechanosensation are of vital importance in animals. We examined the effects of ionizing radiation (IR) on locomotory behavior and mechanosensation using a model organism, the nematode Caenorhabditis elegans. Bacterial mechanosensation in C. elegans induces the dopamine-mediated slowing of locomotion in the presence of bacteria (food), known as the basal slowing response. We previously reported an IR-induced reduction of locomotory rate in the absence of food. In the present study, we observed a similar IR-induced reduction of locomotory rate in the cat-2 mutant, which is defective in bacterial mechanosensation. The dose response pattern of the locomotory rate in the presence of food was relatively flat in wild-type animals, but not in cat-2 mutants. This suggests that the dopamine system, which is related to bacterial mechanosensation in C. elegans, might have a dominant effect on locomotory rate in the presence of food, which masks the effects of other stimuli. Moreover, we found that the behavioral responses of hydrogen peroxide-exposed wild-type animals are similar to those of IR-exposed animals. Our findings suggest that the IR-induced reduction of locomotory rate in the absence of food is mediated by a different pathway from that for bacterial mechanosensation, at least partially through IR-produced hydrogen peroxide.

A synaptic DEG/ENaC ion channel mediates learning in C. elegans by facilitating dopamine signalling

An important component of learned behaviour is the ability to forecast positive or negative outcomes based on specific sensory cues. Predictive capacity is typically manifested by appropriate behavioural patterning. However, the molecular mechanisms underlying behavioural plasticity are poorly understood. Caenorhabditis elegans displays experience-dependent behavioural responses by associating distinct environmental signals. We find that ASIC-1, a member of the degenerin/epithelial sodium channel family, which localizes at presynaptic terminals of dopaminergic neurons, is required for associative learning in C. elegans. ASIC-1 functions in these neurons to amplify normal dopaminergic signalling, necessary for associative learning. Our results reveal a novel role of DEG/ENaC ion channels in neuronal communication by enhancing the activity of dopaminergic synapses. Similar mechanisms may facilitate synaptic plasticity in vertebrates.

Catalases of Aspergillus fumigatus and Inflammation in Aspergillosis

The article describes various features of aspergillosis and a discussed the role of calatases produced by Aspergillus fumigatus during infection. Since a large body of invasive Aspergillus infection occurs as an opportunistic infection in variously impaired defense mechanisms, there is a wide spectrum of histopathological features of lesions demonstrated at the site of infection. Accordingly, histopathology of the lesions can be understood as a phenotypical representation of interaction between differently impaired functions of neutrophils and macrophages and virulence factors of invading Aspergilli. Consideration of previous pathological knowledge regarding infection and inflammation provides much important information to predict the pathophysiology of a patient. Meanwhile, detoxification of hydrogen peroxide by catalases has been proposed as a way to overcome this host response. A. fumigatus produces three active catalases, one from conidia and two from mycelia. CatAp, a spore specific monofunctional catalase, is resistant to heat and metal ions. In spite of their increased sensitivity to H(2)O(2), killing of catA conidia by alveolar macrophages, virulence in animals was similar to wild type conidia. In contrast to mycelial Cat1p, and CatAp catalases, the mycelial Cat2p is a bifunctional catalase-peroxidase enzyme and is also sensitive to heat, metal ions and detergent. Surprisingly, the mycelium of the double cat1 cat2 mutant with no catalase activity has only a slightly increased sensitivity to H(2)O(2) and was as sensitive to the killing of polymorphonuclear neutrophils as the wild type strain. However, it showed a delayed infection in the rat model of aspergillosis compared to the wild type strain. Consequently, it should be emphasized that conidial catalase is not a virulence factor but that mycelial catalases transiently protect the fungus from the host defence reactions.

Dopamine modulates the plasticity of mechanosensory responses in Caenorhabditis elegans.

Dopamine-modulated behaviors, including information processing and reward, are subject to behavioral plasticity. Disruption of these behaviors is thought to support drug addictions and psychoses. The plasticity of dopamine-mediated behaviors, for example, habituation and sensitization, are not well understood at the molecular level. We show that in the nematode Caenorhabditis elegans, a D1-like dopamine receptor gene (dop-1) modulates the plasticity of mechanosensory behaviors in which dopamine had not been implicated previously. A mutant of dop-1 displayed faster habituation to nonlocalized mechanical stimulation. This phenotype was rescued by the introduction of a wild-type copy of the gene. The dop-1 gene is expressed in mechanosensory neurons, particularly the ALM and PLM neurons. Selective expression of the dop-1 gene in mechanosensory neurons using the mec-7 promoter rescues the mechanosensory deficit in dop-1 mutant animals. The tyrosine hydroxylase-deficient C. elegans mutant (cat-2) also displays these specific behavioral deficits. These observations provide genetic evidence that dopamine signaling modulates behavioral plasticity in C. elegans.