Lauritsenkornum4609

Wang et al. (2020) show that binding of the second messenger ppGpp to inosine-guanosine kinase (Gsk) in E. coli modulates the levels of the key metabolite phosphoribosyl pyrophosphate (pRpp), decreasing purine synthesis to favor amino acid synthesis during stress adaptation.Spatial orientation requires the execution of lateralized movements and a change in the animal's heading in response to multiple sensory modalities. While much research has focused on the circuits for sensory integration, chiefly to the midbrain superior colliculus (SC), the downstream cells and circuits that engage adequate motor actions have remained elusive. see more Furthermore, the mechanisms supporting trajectory changes are still speculative. Here, using transneuronal viral tracings in mice, we show that brainstem V2a neurons, a genetically defined subtype of glutamatergic neurons of the reticular formation, receive putative synaptic inputs from the contralateral SC. This makes them a candidate relay of lateralized orienting commands. We next show that unilateral optogenetic activations of brainstem V2a neurons in vivo evoked ipsilateral orienting-like responses of the head and the nose tip on stationary mice. When animals are walking, similar stimulations impose a transient locomotor arrest followed by a change of trajectory. Third, we reveal that these distinct motor actions are controlled by dedicated V2a subsets each projecting to a specific spinal cord segment, with at least (1) a lumbar-projecting subset whose unilateral activation specifically controls locomotor speed but neither impacts trajectory nor evokes orienting movements, and (2) a cervical-projecting subset dedicated to head orientation, but not to locomotor speed. Activating the latter subset suffices to steer the animals' directional heading, placing the head orientation as the prime driver of locomotor trajectory. V2a neurons and their modular organization may therefore underlie the orchestration of multiple motor actions during multi-faceted orienting behaviors.The gynoecium is derived from the fusion of carpels and is considered to have evolved from a simple setup followed by adaptive adjustment in cell type and tissue distribution to facilitate efficient sexual reproduction [1, 2]. As a sequence of the adjustment, the apical gynoecium differentiates into a stigma and a style. Both the structural patterning and functional specification of the apical gynoecium are critical for plant fertility [3, 4]. However, how the fine structures of the apical gynoecium are established at the interface interacting with pollen and pollen tubes remain to be elucidated. Here, we report a novel angiosperm-specific gene family, STIGMA AND STYLE STYLIST 1-3 (SSS1, SSS2, and SSS3). The SSS1 expresses predominately in the transmitting tract tissue of style, SSS2 expresses intensively in stigma, and SSS3 expresses mainly in stylar peripheral region round the transmitting tract. SSSs coregulate the patterning of the apical gynoecium via controlling cell expansion or elongation. Both the architecture and function of apical gynoecium can be affected by the alteration of SSS expression, indicating their critical roles in the establishment of a proper female interface for communication with pollen tubes. The NGATHA3 (NGA3) transcription factor [5, 6] can directly bind to SSSs promoter and control SSSs expression. Overexpression of SSSs could rescue the stylar defect of nga1nga3 double mutant, indicating their context in the same regulatory pathway. Our findings reveal a novel molecular mechanism responsible for patterning the fine architecture of apical gynoecium and establishing a proper interface for pollen tube growth, which is therefore crucial for plant sexual reproduction.EB1 was discovered 25 years ago as a binding partner of the tumor suppressor adenomatous polyposis coli (APC) [1]; however, the significance of EB1-APC interactions has remained poorly understood. EB1 functions at the center of a network of microtubule end-tracking proteins (+TIPs) [2-5], and APC binding to EB1 promotes EB1 association with microtubule ends and microtubule stabilization [6, 7]. Whether EB1 interactions govern functions of APC beyond microtubule regulation has not been explored. The C-terminal basic domain of APC (APC-B) directly nucleates actin assembly, and this activity is required in vivo for directed cell migration and for maintaining normal levels of F-actin [8-10]. Here, we show that EB1 binds APC-B and inhibits its actin nucleation function by blocking actin monomer recruitment. Consistent with these biochemical observations, knocking down EB1 increases F-actin levels in cells, and this can be rescued by disrupting APC-mediated actin nucleation. Conversely, overexpressing EB1 decreases F-actin levels and impairs directed cell migration without altering microtubule organization and independent of its direct binding interactions with microtubules. Overall, our results define a new function for EB1 in negatively regulating APC-mediated actin assembly. Combining these findings with other recent studies showing that APC interactions regulate EB1-dependent effects on microtubule dynamics [7], we propose that EB1-APC interactions govern bidirectional cytoskeletal crosstalk by coordinating microtubule and actin dynamics.In spite of the positive effects of bacteria on health, certain species are harmful, and therefore, animals must weigh nutritional benefits against negative post-ingestion consequences and adapt their behavior accordingly. Here, we use Drosophila to unravel how the immune system communicates with the brain, enabling avoidance of harmful foods. Using two different known fly pathogens, mildly pathogenic Erwinia carotovora (Ecc15) and highly virulent Pseudomonas entomophila (Pe), we analyzed preference behavior in naive flies and after ingestion of either of these pathogens. Although survival assays confirmed the harmful effect of pathogen ingestion, naive flies preferred the odor of either pathogen to air and also to harmless mutant bacteria, suggesting that flies are not innately repelled by these microbes. By contrast, feeding assays showed that, when given a choice between pathogenic and harmless bacteria, flies-after an initial period of indifference-shifted to a preference for the harmless strain, a behavior that lasted for several hours.