Hormone activities and the cell cycle machinery in immunity-triggered growth inhibition.

Biotic stress and diseases caused by pathogen attack pose threats in crop production and significantly reduce crop yields. Enhancing immunity against pathogens is therefore of outstanding importance in crop breeding. However, this must be balanced, as immune activation inhibits plant growth. This immunity-coupled growth trade-off does not support resistance but is postulated to reflect the reallocation of resources to drive immunity. There is, however, increasing evidence that growth-immunity trade-offs are based on the reconfiguration of hormone pathways, shared by growth and immunity signalling. Studies in roots revealed the role of hormones in orchestrating growth across different cell types, with some hormones showing a defined cell type-specific activity. This is apparently highly relevant for the regulation of the cell cycle machinery and might be part of the growth-immunity cross-talk. Since plants are constantly exposed to Immuno-activating microbes under agricultural conditions, the transition from a growth to an immunity operating mode can significantly reduce crop yield and can conflict our efforts to generate next-generation crops with improved yield under climate change conditions. By focusing on roots, we outline the current knowledge of hormone signalling on the cell cycle machinery to explain growth trade-offs induced by immunity. By referring to abiotic stress studies, we further introduce how root cell type-specific hormone activities might contribute to growth under immunity and discuss the feasibility of uncoupling the growth-immunity cross-talk.

Housing helpful invaders: the evolutionary and molecular architecture underlying plant root-mutualist microbe interactions.

Plant root rhizosphere interactions with mutualistic microbes are diverse and numerous, having evolved over time in response to selective pressures on plants to attain anchorage and nutrients. These relationships can be considered to be formed through a combination of architectural connections: molecular architecture interactions that control root-microbe perception and regulate the balance between host and symbiont and developmental architecture interactions that enable the microbes to be 'housed' in the root and enable the exchange of compounds. Recent findings that help to understand the common architecture that exists between nodulation and mycorrhizal interactions, and how this architecture could be re-tuned to develop new symbioses, are discussed here.

Effects of electrical stimulation of efferent olivocochlear neurons on cat auditory-nerve fibers. III. Tuning curves and thresholds at CF.

In order to study the effects of efferent activity, olivocochlear efferents were stimulated with an electrode in the fourth ventricle at the decussation of the crossed olivocochlear bundle (midline-OCB stimulation) or with an electrode at the brainstem origin of medial efferents (MOC stimulation). Tuning curves, or similar measures of threshold, were obtained from auditory-nerve fibers in the presence or absence of efferent stimulation. Efferent stimulation raised the thresholds of fibers for tones at the characteristic frequency (CF) by an amount which varied with the spontaneous rate (SR) of the auditory-nerve fiber. On the average, high-SR fibers had the smallest threshold shifts, and low-SR fibers had the largest threshold shifts. The distribution of threshold shifts as a function of CF peaked at CFs of 3-8 kHz for high-SR and medium-SR fibers but appeared to peak at higher CFs for low-SR fibers. Within the high-SR or medium-SR groups, the fibers with the lowest thresholds had the largest threshold shifts. Efferent stimulation decreased the Q20 of the tuning curves from most fibers (i.e. it made the tuning curves wider), but increased the Q20 from some fibers with CFs below 2 kHz. For fibers with CFs above 4 kHz, efferent stimulation shifted the tuning-curve tails to higher sound levels by about 1 dB on the average. The qualitative patterns of the effects due to midline-OCB stimulation or to MOC stimulation were similar. The distribution of high-SR threshold shifts vs. CF appears to be displaced apically in the cochlea compared to the distribution of MOC endings on outer hair cells. This can be understood in terms of efferent activity depressing basilar membrane motion and affecting regions at, and apical to, the activated efferent synapses. To explain the low-SR threshold shifts, an additional way in which efferent activity inhibits responses appears to be required. The data are consistent with one function of the medial efferents being to raise the thresholds of auditory-nerve fibers and thereby adjust the effective range of the auditory system.

Effects of electrical stimulation of efferent olivocochlear neurons on cat auditory-nerve fibers. II. Spontaneous rate.

In order to increase our understanding of cochlear mechanisms, we measured changes in the rate of spontaneous firing (SR) of single auditory-nerve fibers in response to the stimulation of medial olivocochlear efferents in cats. During the first second of efferent stimulation, SR was depressed by up to 35%, except in one very sensitive animal in which depressions up to 80% were found. With data from this aberrant cat excluded, the SR depression, on the average, increased as auditory-nerve fiber sensitivity increased, increased as the original SR decreased (data were not obtained for SRs less than two spikes/sec), and had a broad maximum at CFs of about 10 kHz. After the efferent stimulation was turned off, there was an "overshoot" in which the SR increased past the original rate in some fibers. The "overshoot" was larger for fibers with lower SRs and for fibers which showed larger "adaptation" in the efferent-induced depression of SR. The data on SR depression during efferent stimulation are consistent with two hypotheses: (1) that the stronger than usual efferent suppression of "spontaneous" rate found in some very sensitive fibers occurs because the "spontaneous" firing was, in part, a response to sound, and (2) that "true spontaneous" firing is reduced by the efferent-induced hyperpolarization of outer hair cells (OHCs) being electrically coupled through the endocochlear potential to inner hair cells (IHCs). It is suggested that (1) the efferent-induced suppression of "true spontaneous" activity is largest at CFs near 10 kHz because this CF region receives the greatest OHC innervation from medial efferents and the efferent-induced change in OHCs is electrically coupled to IHCs, whereas (2) the efferent suppression of responses to sound is largest at lower CFs because the efferent endings on OHCs act to decrease the motion of the basilar membrane and this change is propagated apically from the active efferent synapses on OHCs.

Effects of electrical stimulation of efferent olivocochlear neurons on cat auditory-nerve fibers. I. Rate-level functions.

In previous studies describing the effects of electrically stimulating the olivocochlear bundle, it seems possible that both medial and lateral (MOC and LOC) efferents may have been stimulated. To selectively stimulate MOC efferents, we used an electrode placed at the origin of the MOC efferents in the brainstem (MOC stimulation). For comparison, a stimulating electrode was placed in the fourth ventricle at the decussation of the crossed olivocochlear bundle where both MOC and LOC efferents are present (midline-OCB stimulation). Rate versus sound level functions from auditory-nerve fibers were obtained with and without efferent stimulation. Stimulation at either location shifted rate vs. level functions to higher sound levels and depressed the rate in the plateau. For fibers with high spontaneous rates, the level shifts and plateau depressions had slightly different distributions as a function of characteristic frequency. The average amplitudes of these effects were largest for midline-OCB stimulation, next largest for crossed MOC stimulation and smallest for uncrossed MOC stimulation. The qualitative pattern of the effects, however, did not depend on the location of the stimulus electrode. The amplitudes of the efferent-induced effects were different for auditory-nerve fibers with different spontaneous rates (by as much as a factor of three for the plateau depression). The results support several hypotheses: (1) the effects of midline-OCB stimulation are due only to the action of MOC efferents, (2) individual crossed and uncrossed MOC fibers produce similar effects, and (3) efferents differentially change the information carrying properties of auditory-nerve fibers in different spontaneous-rate categories. These results, taken together with anatomical data in the literature, are consistent with the hypothesis that, in the cat, MOC and midline-OCB stimulation have their effect solely through synapses on outer hair cells. The data are consistent with the hypothesis that the level shifts are produced by MOC efferents acting on outer hair cells to reduce the mechanical stimulus to inner hair cells. It seems likely that some other mechanism is required to produce the plateau depressions, at least for auditory-nerve fibers with high spontaneous rates.

Effects of electrical stimulation of medial olivocochlear neurons on ipsilateral and contralateral cochlear responses.

Recent anatomical evidence has cast doubt on the interpretation of the neural elements involved in past experiments in which efferents were electrically stimulated. To separate effects produced by medial olivocochlear (MOC) efferents from effects produced by lateral olivocochlear (LOC) efferents, MOC efferents were selectively stimulated by an electrode in the region of the MOC cell bodies in cats. For comparison, efferents were also stimulated with an electrode in the fourth ventricle (OCB stimulation, previously called COCB stimulation). MOC stimulation and fourth-ventricle OCB stimulation both produced qualitatively similar results bilaterally in that auditory-nerve compound action potential (N1) and endocochlear potential were reduced, and cochlear microphonic (CM) was increased. Both efferent-induced changes were affected in similar ways by changes in shock parameters, and were blocked by strychnine. At low sound levels, the decrease in N1 amplitude was approximately equivalent to a shift (decrease) in sound level but the change in N1 latency was not. The ratio of the CM increase to the N1 sound-level shift was independent of shock level or location. MOC stimulation typically produced an N1 sound-level shift of 11-16 dB in the contralateral ear and 4-7 dB in the ipsilateral ear. The ratio of these shifts almost equals the ratio of MOC neurons which had cell bodies on the stimulating-electrode side. Previous results reported by others with 'UOCB stimulation' now seem attributable to excitation of uncrossed MOC efferents rather than to excitation of uncrossed LOC efferents as previously thought. There is no effect reported in the literature or seen by us which can definitely be attributed to LOC neurons. Fourth-ventricle OCB stimulation typically produced an N1 sound-level shift in both ears of 19-22 dB which is approximately the sum of the crossed and uncrossed MOC shifts. Considering also that many uncrossed-MOC fibers course close to the midline (i.e. near the stimulating electrode), it seems likely that fourth-ventricle OCB stimulation excites both crossed and uncrossed MOC efferents. Referring to such stimulation in the cat as 'COCB stimulation' is therefore inaccurate and may lead to wrong conclusions about the functional role of various components of the olivocochlear fibers.

Effects of crossed-olivocochlear-bundle stimulation on cat auditory nerve fiber responses to tones.

Phase, synchronization index, and average firing rate were calculated from period histograms of tone burst responses obtained from sound level series with and without electrical stimulation of the cross-olivocochlear-bundle (COCB). For most fibers, at low sound levels, COCB stimulation shifted the rate and synchronization index level functions up in sound level but did not shift the phase-level function in the same way. These effects can be accounted for if the stage at which the COCB acts precedes the stage at which analog signals are changed into neural firing patterns with a given rate and synchronization index, but does not precede the stage at which the level dependence of phase is introduced. Some level series show an abrupt phase change and "dips" in rate and synchronization-index level functions at high sound levels. COCB stimulation shifted these abrupt phase changes and dips down in sound level and usually had little effect at sound levels above these abrupt phase changes and dips. The following explanatory hypothesis is developed: excitation of an auditory-nerve fiber is the result of two factors which are out of phase and have different growth functions. The two factors cancel when they are equal in amplitude producing the dips and phase changes. COCB stimulation reduces the more sensitive factor but does not change the other factor so the two factors cancel at a lower sound level with COCB stimulation.