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Geyer, L.

Publications and source records attributed to Geyer, L..

2 recordsLinked to original sources

CYSTM1, a drought-responsive cysteine-rich transmembrane module protein, negatively affects drought tolerance in Arabidopsis thaliana

Drought stress represents a major challenge for plant growth and survival, requiring coordinated regulation of physiological and molecular responses to maintain water balance. The cysteine-rich transmembrane module (CYSTM) family comprises a highly conserved group of small proteins whose functions in plant stress adaptation remain largely unknown. Here, we identified CYSTM1 (AT1G05340) as a drought-responsive gene in Arabidopsis thaliana whose expression increased in response to prolonged water deficit, osmotic stress, high salinity, and abscisic acid (ABA). Analysis of a loss-of-function T-DNA insertion mutant (cystm1) showed no growth phenotype compared to the wild-type under well-watered conditions. However, the mutant plants exhibited enhanced drought tolerance, whereas independent complementation lines restored the wild-type phenotype. The improved drought performance of the cystm1 plants was associated with reduced stomatal aperture and decreased transpiration. Mutant plants also displayed an enhanced seedling establishment under osmotic stress conditions. Loss of CYSTM1 altered ABA-associated responses at physiological and transcriptional level, resulting in reduced sensitivity to exogenous ABA and attenuated expression of ABA- and drought-responsive genes during water deficit. Co-expression analysis showed that genes with expression pattern similar to CYSTM1 include many genes related to drought response as well as other members of the CYSTM family. Further expression analyses revealed selective transcriptional reprogramming within the CYSTM family following the loss of CYSTM1, suggesting crosstalk or functional interdependence within the CYSTM gene family. Collectively, these findings identify CYSTM1 as a novel negative effector of drought tolerance.

plant biology↗

A collicular somatostatinergic circuit gates sensory access to action

Animals are exposed to far more sensory information than can be converted into action and must prioritise behaviourally salient events. Although salience is commonly studied as modulation of sensory representations, stimulus prioritisation may also arise at premotor stages, through mechanisms that regulate the readiness of action-generating circuits to be recruited by sensory input. The superior colliculus links visual signals to spatially directed orienting and contains Pitx2-expressing spatial-motor modules that coordinate spatially targeted actions, providing a substrate for premotor regulation of sensory access to action. However, the circuit elements that regulate this access remain unknown. Here we identify an intersectionally targeted population of somatostatin-expressing inhibitory neurons in the mouse superior colliculus that is, at the population level, suppressed during orienting movements and visual stimulation. These neurons provide input to Pitx2-expressing spatial-motor modules, and their optogenetic silencing increased retinally evoked firing in Pitx2 neurons, showing that somatostatinergic inhibition constrains the visual recruitment of collicular motor output. Increasing somatostatinergic tone reduced interception of low- and intermediate-contrast visual targets while sparing responses to high-contrast targets, consistent with graded control of sensory access to action. Cholecystokinin-expressing inhibitory neurons and multiple cortical and subcortical regions provide anatomical input to the somatostatinergic population, identifying candidate routes for local and context-dependent regulation. Together, these findings establish somatostatinergic inhibition as a premotor control point that regulates the readiness of spatial-motor circuits for sensory recruitment and identify a circuit architecture through which the behavioural impact of salient sensory events could be regulated downstream of sensory encoding.

neuroscience↗