There is increasing evidence that competent handling of social interactions among conspecifics has positive effects on individual fitness. While individual variation in social competence has been appreciated, the role of long-term experience in the acquisition of superior social skills has received less attention. With the goal of promoting further research, we integrate knowledge across disciplines to assess social expertise, defined as the characteristics, skills and knowledge allowing individuals with extensive social experience to perform significantly better than novices on a given social task. We focus on three categories of social behaviour. First, animals can gain from adjusting social behaviour towards individually recognised conspecifics that they interact with on a regular basis. For example, there is evidence that some territorial animals individually recognise their neighbours and modify their social interactions based on experience with each neighbour. Similarly, individuals in group-living species learn to associate with specific group members based on their expected benefits from such social connections. Individuals have also been found to devote considerable time and effort to learning about the spatial location and timing of sexual receptivity of opposite-sex neighbours to optimise reproduction. Second, signallers can enhance their signals, and receivers can refine their response to signals with experience. In many birds and insects, individuals can produce more consistent signals with experience, and females across a wide taxonomic range can adaptively adjust mating preferences after perceiving distinct male signals. Third, in many species, individuals that succeed in reproducing encounter the novel, complex task of caring for vulnerable offspring. Evidence from a few species of mammals indicates that mothers improve in providing for and protecting their young over successive broods. Finally, for social expertise to evolve, heritable variation in social expertise has to be positively associated with fitness. Heritable variation has been shown in traits contributing to social expertise including social attention, empathy, individual recognition and maternal care. There are currently limited data associating social expertise with fitness, most likely owing to sparse research effort. Exceptions include maternal care, signal refinement, and familiarity with neighbours and group members. Overall, there is evidence that individuals in many species keep refining their social skills with experience throughout life. Hence we propose promising lines of research that can quantify more thoroughly the development of social expertise and its effects on fitness.

The abscission of floral organs and emergence of lateral roots in Arabidopsis is regulated by the peptide ligand inflorescence deficient in abscission (IDA) and the receptor protein kinases HAESA (HAE) and HAESA-like 2 (HSL2). During these cell separation processes, the plant induces defense-associated genes to protect against pathogen invasion. However, the molecular coordination between abscission and immunity has not been thoroughly explored. Here, we show that IDA induces a release of cytosolic calcium ions (Ca2+) and apoplastic production of reactive oxygen species, which are signatures of early defense responses. In addition, we find that IDA promotes late defense responses by the transcriptional upregulation of genes known to be involved in immunity. When comparing the IDA induced early immune responses to known immune responses, such as those elicited by flagellin22 treatment, we observe both similarities and differences. We propose a molecular mechanism by which IDA promotes signatures of an immune response in cells destined for separation to guard them from pathogen attack.

G protein-coupled receptors (GPCRs) are a large family of cell surface receptors that play a critical role in nervous system function by transmitting signals between cells and their environment. They are involved in many, if not all, nervous system processes, and their dysfunction has been linked to various neurological disorders representing important drug targets. This overview emphasises the GPCRs of the nervous system, which are the research focus of the members of ERNEST COST action (CA18133) working group \'Biological roles of signal transduction\'. First, the (patho)physiological role of the nervous system GPCRs in the modulation of synapse function is discussed. We then debate the (patho)physiology and pharmacology of opioid, acetylcholine, chemokine, melatonin and adhesion GPCRs in the nervous system. Finally, we address the orphan GPCRs, their implication in the nervous system function and disease, and the challenges that need to be addressed to deorphanize them.

Platelets are small anucleate blood cells supporting vascular function. They circulate in a quiescent state monitoring the vasculature for injuries. Platelets adhere to injury sites and can be rapidly activated to secrete granules and to form platelet/platelet aggregates. These responses are controlled by signalling networks that include G proteins and their regulatory guanine nucleotide exchange factors (GEFs) and GTPase-activating proteins (GAPs). Recent proteomics studies have revealed the complete spectrum of G proteins, GEFs, and GAPs present in platelets. Some of these proteins are specific for platelets and very few have been characterised in detail. GEFs and GAPs play a major role in setting local levels of active GTP-bound G proteins in response to activating and inhibitory signals encountered by platelets. Thus, GEFs and GAPs are highly regulated themselves and appear to integrate G protein regulation with other cellular processes. This review focuses on GAPs of small G proteins of the Arf, Rab, Ras, and Rho families, as well as of heterotrimeric G proteins found in platelets.

Physiological processes that govern the normal functioning of mammalian cells are regulated by a myriad of signalling pathways. Mammalian mitogen-activated protein (MAP) kinases constitute one of the major signalling arms and have been broadly classified into four groups that include extracellular signal-regulated protein kinase (ERK), c-Jun N-terminal kinase (JNK), p38, and ERK5. Each signalling cascade is governed by a wide array of external and cellular stimuli, which play a critical part in mammalian cells in the regulation of various key responses, such as mitogenic growth, differentiation, stress responses, as well as inflammation. This evolutionarily conserved MAP kinase signalling arm is also important for metabolic maintenance, which is tightly coordinated via complicated mechanisms that include the intricate interaction of scaffold proteins, recognition through cognate motifs, action of phosphatases, distinct subcellular localisation, and even post-translational modifications. Aberration in the signalling pathway itself or their regulation has been implicated in the disruption of metabolic homeostasis, which provides a pathophysiological foundation in the development of metabolic syndrome. Metabolic syndrome is an umbrella term that usually includes a group of closely associated metabolic diseases such as hyperglycaemia, hyperlipidaemia, and hypertension. These risk factors exacerbate the development of obesity, diabetes, atherosclerosis, cardiovascular diseases, and hepatic diseases, which have accounted for an increase in the worldwide morbidity and mortality rate. This review aims to summarise recent findings that have implicated MAP kinase signalling in the development of metabolic diseases, highlighting the potential therapeutic targets of this pathway to be investigated further for the attenuation of these diseases.

Social interactions are inevitable in the lives of most animals, since most essential behaviours require interaction with conspecifics, such as mating and competing for resources. Non-avian reptiles are typically viewed as solitary animals that predominantly use their vision and olfaction to communicate with conspecifics. Nevertheless, in recent years, evidence is mounting that some reptiles can produce sounds and have the potential for acoustic communication. Reptiles that can produce sound have an additional communicative channel (in addition to visual/olfactory channels), which could suggest they have a higher communicative complexity, the evolution of which is assumed to be driven by the need of social interactions. Thus, acoustic reptiles may provide an opportunity to unveil the true social complexity of reptiles that are usually thought of as solitary. This review aims to reveal the hidden social interactions behind the use of sounds in non-avian reptiles. Our review suggests that the potential of vocal and acoustic communication and the complexity of social interactions may be underestimated in non-avian reptiles, and that acoustic reptiles may provide a great opportunity to uncover the coevolution between sociality and communication in non-avian reptiles. This article is part of the theme issue \'The power of sound: unravelling how acoustic communication shapes group dynamics\'.

Plants growing in dense vegetation stands need to flexibly position their photosynthetic organs to ensure optimal light capture in a competitive environment. They do so through a suite of developmental responses referred to as the shade avoidance syndrome. Belowground, root development is also adjusted in response to aboveground neighbour proximity. Canopies are dynamic and complex environments with heterogenous light cues in the far-red, red, blue and UV spectrum, which can be perceived with photoreceptors by spatially separated plant tissues. Molecular regulation of plant architecture adjustment via PHYTOCHROME-INTERACTING FACTOR (PIF) transcription factors and growth-related hormones such as auxin, gibberellic acid, brassinosteroids and abscisic acid were historically studied without much attention to spatial or tissue-specific context. Recent developments and technologies have, however, sparked strong interest in spatially explicit understanding of shade avoidance regulation. Other environmental factors such as temperature and nutrient availability interact with the molecular shade avoidance regulation network, often depending on the spatial location of the signals, and the responding organs. Here, we aim to review recent advances in how plants respond to heterogenous light cues and integrate these with other environmental signals.

The phosphoinositide-3 kinase (PI3K), a heterodimeric enzyme, plays a pivotal role in cellular metabolism and survival. Its deregulation is associated with major human diseases, particularly cancer. The p85 regulatory subunit of PI3K binds to the catalytic p110 subunit via its C-terminal domains, stabilising it in an inhibited state. Certain Src homology 3 (SH3) domains can activate p110 by binding to the proline-rich (PR) 1 motif located at the N-terminus of p85. However, the mechanism by which this N-terminal interaction activates the C-terminally bound p110 remains elusive. Moreover, the intrinsically poor ligand selectivity of SH3 domains raises the question of how they can control PI3K. Combining structural, biophysical, and functional methods, we demonstrate that the answers to both these unknown issues are linked: PI3K-activating SH3 domains engage in additional \"tertiary\" interactions with the C-terminal domains of p85, thereby relieving their inhibition of p110. SH3 domains lacking these tertiary interactions may still bind to p85 but cannot activate PI3K. Thus, p85 uses a functional selection mechanism that precludes nonspecific activation rather than nonspecific binding. This separation of binding and activation may provide a general mechanism for how biological activities can be controlled by promiscuous protein-protein interaction domains.

The elucidation of the molecular basis underlying plant-pathogen interactions is imperative for the development of sustainable resistance strategies against pathogens. Plants employ a dual-layered immunological detection and response system wherein cell surface-localized Pattern Recognition Receptors (PRRs) and intracellular Nucleotide-Binding Leucine-Rich Repeat Receptors (NLRs) play pivotal roles in initiating downstream signalling cascades in response to pathogen-derived chemicals. Pattern-Triggered Immunity (PTI) is associated with PRRs and is activated by the recognition of conserved molecular structures, known as Pathogen-Associated Molecular Patterns. When PTI proves ineffective due to pathogenic effectors, Effector-Triggered Immunity (ETI) frequently confers resistance. In ETI, host plants utilize NLRs to detect pathogen effectors directly or indirectly, prompting a rapid and more robust defense response. Additionally epigenetic mechanisms are participating in plant immune memory. Recently developed technologies like CRISPR/Cas9 helps in exposing novel prospects in plant pathogen interactions. In this review we explore the fascinating crosstalk and cooperation between PRRs and NLRs. We discuss epigenomic processes and CRISPR/Cas9 regulating immune response in plants and recent findings that shed light on the coordination of these defense layers. Furthermore, we also have discussed the intricate interactions between the salicylic acid and jasmonic acid signalling pathways in plants, offering insights into potential synergistic interactions that would be harnessed for the development of novel and sustainable resistance strategies against diverse group of pathogens.

Behavioural regulation in insect societies remains a fundamental question in sociobiology. In hymenopteran societies, the queen plays a crucial role in regulating group behaviour by affecting individual behaviour and physiology through modulation of worker gene expression. Honey bee (Apis mellifera) queens signal their presence via queen mandibular pheromone (QMP). While QMP has been shown to influence behaviour and gene expression of young workers, we know little about how these changes translate in older workers. The effects of the queen pheromone could have prolonged molecular impacts on workers that depend on an early sensitive period. We demonstrate that removal of QMP impacts long-term gene expression in the brain and antennae in foragers that were treated early in life (1 day post emergence), but not when treated later in life. Genes important for division of labour, learning, chemosensory perception and ageing were among those differentially expressed in the antennae and brain tissues, suggesting that QMP influences diverse physiological and behavioural processes in workers. Surprisingly, removal of QMP did not have an impact on foraging behaviour. Overall, our study suggests a sensitive period early in the life of workers, where the presence or absence of a queen has potentially life-long effects on transcriptional activity.