Changes in melon plant phytochemistry impair Aphis gossypii growth and weight under elevated CO2

Elevated CO2 (eCO2) modifies plant primary and secondary metabolism that subsequently impacts herbivore insect performance due to changes in its nutritional requirements. This laboratory study evaluated interactions between Aphis gossypii Glover (Hemiptera: Aphididae) and melon (Cucumis melo L., Cucurbitaceae), previously acclimated two or six weeks to different CO2 levels, eCO2 (700 ppm) or ambient CO2 (400 ppm). Under eCO2, melon plants decreased nitrogen foliar concentration and increased carbon to nitrogen ratio, independently of acclimation period, significantly reducing the content of some amino acids (alanine, asparagine, glycine, isoleucine, lysine, serine, threonine, and valine) and increasing the carbohydrate (sucrose) content in melon leaves. The dilution in some essential amino acids for aphid nutrition could have aggravated the reduction in A. gossypii population growth reared on melon previously acclimated two weeks to eCO2, as well as the loss of aphid body mass from two successive generations of A. gossypii reared under eCO2 on plants previously acclimated two or six weeks to eCO2. The response to eCO2 of phloem feeders, such as aphids, is actually variable, but this study highlights a negative response of A. gossypii to this climate change driver. Potential implications on control of this pest in a global change scenario are discussed.

Pan-cancer screen for mutations in non-coding elements with conservation and cancer specificity reveals correlations with expression and survival

Cancer develops by accumulation of somatic driver mutations, which impact cellular function. Non-coding mutations in non-coding regulatory regions can now be studied genome-wide and further characterized by correlation with gene expression and clinical outcome to identify driver candidates. Using a new two-stage procedure, called ncDriver, we first screened 507 ICGC whole-genomes from ten cancer types for non-coding elements, in which mutations are both recurrent and have elevated conservation or cancer specificity. This identified 160 significant non-coding elements, including theTERTpromoter, a well-known non-coding driver element, as well as elements associated with known cancer genes and regulatory genes (e.g.,PAX5,TOX3,PCF11,MAPRE3). However, in some significant elements, mutations appear to stem from localized mutational processes rather than recurrent positive selection in some cases. To further characterize the driver potential of the identified elements and shortlist candidates, we identified elements where presence of mutations correlated significantly with expression levels (e.g.TERTandCDH10) and survival (e.g.CDH9andCDH10) in an independent set of 505 TCGA whole-genome samples. In a larger pan-cancer set of 4,128 TCGA exomes with expression profiling, we identified mutational correlation with expression for additional elements (e.g., nearGATA3,CDC6,ZNF217andCTCFtranscription factor binding sites). Survival analysis further pointed toMIR122, a known marker of poor prognosis in liver cancer. This screen for significant mutation patterns followed by correlative mutational analysis identified new individual driver candidates and suggest that some non-coding mutations recurrently affect expression and play a role in cancer development.

Conditional Rhythmicity and Synchrony in a Bilateral Pair of Bursting Motor Neurons in Aplysia

This investigation examined the activity of a bilateral pair of motor neurons (B67) in the feeding system of Aplysia californica. In isolated ganglia, B67 firing exhibited a highly stereotyped bursting pattern that could be attributed to an underlying TTX-resistant driver potential (DP). Under control conditions, this bursting in the two B67 neurons was infrequent, irregular, and asynchronous. However, bath application of the neuromodulator dopamine (DA) increased the duration, frequency, rhythmicity, and synchrony of B67 bursts. In the absence of DA, depolarization of B67 with injected current produced rhythmic bursting. Such depolarization-induced rhythmic burst activity in one B67, however, did not entrain its contralateral counterpart. Moreover, when both B67s were depolarized to potentials that produced rhythmic bursting, their synchrony was significantly lower than that produced by DA. In TTX, dopamine increased the DP duration, enhanced the amplitude of slow signaling between the two B67s, and increased DP synchrony. A potential source of dopaminergic signaling to B67 was identified as B65, an influential interneuron with bilateral buccal projections. Firing B65 produced bursts in the ipsilateral and contralateral B67s. Under conditions that attenuated polysynaptic activity, firing B65 evoked rapid excitatory postsynaptic potentials in B67 that were blocked by sulpiride, an antagonist of synaptic DA receptors in this system. Finally, firing a single B65 was capable of producing a prolonged period of rhythmic synchronous bursting of the paired B67s. It is proposed that modulatory dopaminergic signaling originating from B65 during consummatory behaviors can promote rhythmicity and bilateral synchrony in the paired B67 motor neurons.

Plateau-Generating Nerve Cells in Helix: Morphological and Electrophysiological Characteristics

We describe the anatomical and electrophysiological characteristics of a group of Helix nerve cells, styled P cells, that generate long-lasting depolarizations in response to repeated stimulations at low frequencies. Four neurones were identified in the perioesophageal ganglia of the snail Helix pomatia. Their structure was determined by intracellular injection of Lucifer Yellow, cobaltlysine or horseradish peroxidase. The soma was found to contain neurosecretory granules. These cells innervated the whole foot muscle and the mantle, but were not involved in muscle movement or locomotion. They may participate in mucus secretion. Upon depolarization they fired Ca2+-dependent spikes; at a critical firing rate (5–6 Hz), the spikes were converted into depolarized plateaus (+10 to +20 mV) lasting for several seconds. The plateau was Ca2+-dependent and persisted in Na+-free saline. It was sustained by a slowly inactivating Ca2+ current that produced a large intracellular Ca2+ accumulation (monitored with the Ca2+- sensitive dye Arsenazo III). The plateau was restricted to the soma and the proximal axon and may act as a driver potential inducing axon firing and prolonging the release of neurosecretory materials. Note: To whom reprint requests should be addressed.

Characterization of Ca current underlying burst formation in lobster cardiac ganglion motorneurons

1. The anterior motorneurons of the cardiac ganglion of Homarus americanus were ligated less than 300 microns from the soma. This removes impulse-generating membrane and sites of synaptic input while preserving the ability of the soma to generate the burst-forming potentials termed "driver potentials" regenerative, slow (250-ms duration) depolarizations (to -20 mV) in response to brief, depolarizing stimuli. At stimulus intervals corresponding to rates of bursting observed in spontaneously active, intact ganglia (0.3-1.2/s), driver potential amplitude increases with increasing stimulus interval. 2. A two-electrode voltage clamp was used to characterize inward current observable from the ligated neurons in tetrodotoxin (TTX)-tetraethylammonium (TEA)-containing salines. The amplitude of inward current shows a hyperbolic relation to [Ca]o that is well fitted by a form of the Michaelis-Menten equation. Inward current is maintained but not augmented when Ca2+ is replaced by Ba2+ or Sr2+. It is concluded that the inward current, to be referred to as ICa, is mediated by voltage-dependent Ca channels. 3. Contamination of ICa by early outward current (IA) was evaluated by addition of 4-aminopyridine (4-AP, 4 mM). In the presence of 4-AP, the net inward current is increased and the potential at which maximum ICa occurs is shifted 10 mV more positive. 4. Subtraction of outward currents recorded in Mn2(+)-containing saline from overall currents in the absence of Mn2+ provided another means to separate inward from outward current. I-V curves from such "Mn-subtracted" records show ICa approaches a saturating value for steps to -5 mV and more depolarized. The time to peak ICa is voltage dependent. The largest inward currents (up to 240 nA) and minimal time to peak (4 ms) are observed for steps from holding potentials of -50 to -60 mV. 5. Decline of ICa during depolarized steps observed in Mn-subtracted records represents inactivation rather than development of competing outward current. Inactivation is slow and incomplete; the rate and fractional amount of inactivation are not directly voltage dependent. Nonsubtracted responses to 500-ms depolarizations to potentials evoking little outward current show that an initial rapid decline of ICa (tau approximately 40 ms) is followed at approximately 80 ms by a slower phase of decline (tau approximately 180 ms). With repetitive clamps, the early phase proved labile.(ABSTRACT TRUNCATED AT 400 WORDS)

Excitatory Effects of Dopamine on the Cardiac Ganglia of the Crabs Portunus Sanguinolentus and Podophthalmus Vigil

1. Dopamine, a cardioexcitor in decapod crustaceans, increased the frequency and/or duration of bursts of action potentials in the semi-isolated cardiac ganglia of two species of crabs. The number of motoneurone action potentials in each burst was increased, which in the intact heart would increase the force and amplitude of heart contraction. 2. The effects were concentration-dependent, with a threshold concentration of 10−8M or lower when dopamine was applied by continuous perfusion. At 5×10−6M, dopamine increased burst frequency by 200%. 3. The main site of dopamine action was the group of four posterior small interneurones which normally function as the pacemaker for the cardiac ganglion system. Effects on the five large motoneurones occurred at higher concentrations. This regional difference in sensitivity was demonstrated by selective applications of dopamine to different parts of the cardiac ganglion and by the use of preparations in which the two ends of the ganglion had been functionally separated by a ligature around the ganglionic trunk. 4. In the small neurones, dopamine was found to stimulate the slow tetrodotoxin-resistant regenerative depolarizations known as driver potentials. The effects on driver potential frequency and train duration were concentration dependent. In one of the two species of crabs, in which electrotonic connections between small and large neurones are strong, large neurone driver potentials were indirectly induced by dopamine. 5. In the tetrodotoxin-treated large motoneurones, dopamine, at a concentration about ten-fold higher than needed to activate the small neurones, decreased the threshold for current-induced driver potentials, and slightly reduced membrane resistance. 6. We suggest that the excitatory action of dopamine on the untreated cardiac ganglion can in large part be accounted for by its action on driver potential production in the small neurones.

Burst reset and frequency control of the neuronal oscillators in the cardiac ganglion of the crab, Portunus sanguinolentus

1. The five large and four small neurones in the cardiac ganglion of the crab, Portunus, are electrotonically coupled and behave as a single relaxation oscillator, exhibiting periodic bursting activity in vitro. Recorded from the large neurone somata, this activity consists of 200-400 ms slow depolarizations called ‘driver potentials’ (Tazaki & Cooke, 1979a), accompanied by attenuated action potentials and EPSP's from small neurone input. 2. There is a strong positive correlation between the duration of the driver potential and the duration of the following interburst interval in the spontaneously active ganglion. This correlation is preserved during prolonged depolarization and hyperpolarization. 3. When a driver potential is prematurely terminated by an injected current pulse, the following interburst interval is shortened in direct proportion to the decrease in driver potential duration. 4. When a driver potential or a burst of high-frequency action potential activity is evoked by a depolarizing current pulse, the cardiac oscillator resets to the point of maximum hyperpolarization of the burst cycle, and the following interburst interval is of normal duration. Resetting following an evoked driver potential is complete. Partial resetting occurs only after short, evoked action potential bursts in the absence of a driver potential. 5. Reset of the oscillator causes phase shifts in the subsequent cycles of activity, which vary with the phase of application and duration of the injected current pulse. Response curves have been constructed for a comprehensive range of durations and intensities of hyperpolarizing and depolarizing current pulses applied at all phases of the oscillator cycle. 6. The phase shifts are composed of contributions from the duration of the current pulse, from the premature initiation of the slow depolarizing pacemaker potential due to early termination of the burst, and from the change in interburst interval correlated with truncation of the driver potential. 7. Considering the cardiac ganglion as a relaxation oscillator, frequencey control by entrainment to periodically applied current pulses was quantitatively predicted from the phase-response curves and experimentally confirmed. 8. A high concentration (10(−5) M) of octopamine can inhibit driver potential activity in the large neurones. This was used to examine possible frequency modulating effects of electrotonic feedback from the large neurone driver potentials onto the small neurone pacemaker activity. 9. The observations are discussed in relation to the ionic model for driver potentials and slow pacemaker potential activity in the cardiac ganglion, as proposed by Tazaki & Cooke (1979a, b).