Development Function Research Articles

К проблеме героя итальянской оратории XVII века

The aim of the article is to examine the phenomenon of the main protagonist from the perspective of his tragic nature as an expression of the concentrated essence of baroque ethics and aesthetics as manifested in the culminating stage of the development of 17th century oratorio (San Giovanni Battista by Alessandro Stradella) and on the stage of the genre’s exhaustion (Agar et Ismaele Esiliati by Alessandro Scarlatti). The principle of “relative clarity” (to use the expression of Heinrich Wölfflin) became fundamental in considering the features of baroque aesthetics in music. This principle manifested itself in various aspects of the oratorio: in its concept, drama, interpretation of the main characters, and the very genre. Conceptually, this principle is expressed in the chief protagonist’s moral hesitation about a decision which was made (as in the oratorios Herode and Abramo). Dramatically, it manifested itself in the move made by the developmental functions upon the expositional ones – as in the oratorio San Giovanni Battista – or in the application of two different focuses of vision on the part of the same protagonist, such as Herode (Herod), Salome, Abramo (Abraham) or Sara (Sarah): this is shown most vividly in the expositions of the first and second acts of the oratorio Agar et Ismaele Esiliati. In the interpretation of the main characters the transmission of the principle of “relative clarity” was demonstrated in the interpersonal conflict: in Stradella’s oratorio, it is directly expressed between John the Baptist, on the one hand, and Herod and Salome, on the other hand, and indirectly – between San Giovanni Battista (John the Baptist), on the other hand, and Herodiade (Herodias) and the Consigliere (Herod’s counselor), on the other hand; in Scarlatti’s work – between Abramo and Sara, on the one hand, and Agar (Hagar) and Ismaele (Ishmael), on the other hand. At the same time, the psychological state of most characters is characterized by explosive emotions, which often reach the level of intrapersonal conflict. In Stradella’s work, Herode experiences such feelings (there are indications that Salome undergoes them in some of their aspects, as well); and in Scarlatti’s oratorio a similar “counter-feeling” (a term coined by Lev Vygotsky) is crystallized in the actions of Abramo. The principle of “relative clarity” was also reflected in a peculiar mutation on the part of the oratorio as a genre, in which the chorus (featuring one of its main attributes) is reduced to a minimal level – as in the oratorio San Giovanni Battista, or is completely absent – as in the oratorio Agar et Ismaele Esiliati. Keywords: Alessandro Stradella, Alessandro Scarlatti, Italian oratorio, tragic, baroque hero, San Giovanni Battista (John the Baptist), Herode, Herodiade, Salome, Abramo, Sara, Agar, Ismaele, intrapersonal conflict, “relative clarity.”

Into the body wall and back out again.

Two analyses of developmental patterning functions of leg and wing genes in a crustacean provide complementary support for the incorporation of proximal leg components into the body wall during the crustacean–insect transition, but lead to duelling models for which portion(s) re-emerged from the body as wings.

Emerging roles of steroid receptor coactivators in stromal cell responses.

Tissue parenchyma is the functional unit of an organ and all of the remaining cells within that organ collectively make up the tissue stroma. The stroma includes fibroblasts, endothelial cells, immune cells, and nerves. Interactions between stromal and epithelial cells are essential for tissue development and healing after injury. These interactions are governed by growth factors, inflammatory cytokines and hormone signaling cascades. The steroid receptor coactivator (SRC) family of proteins includes three transcriptional coactivators that facilitate the assembly of multi-protein complexes to induce gene expression in response to activation of many cellular transcription factor signaling cascades. They are ubiquitously expressed and are especially critical for the developmental function of steroid hormone responsive tissues. The SRCs are overexpressed in multiple cancers including breast, ovarian, prostate and endometrial cancers. In this review, we focus on the role of the SRCs in regulating the functions of stromal cell components responsible for angiogenesis, inflammation and cell differentiation.

Cell non-autonomous requirement of p75 in the development of geniculate oral sensory neurons

During development of the peripheral taste system, oral sensory neurons of the geniculate ganglion project via the chorda tympani nerve to innervate taste buds in fungiform papillae. Germline deletion of the p75 neurotrophin receptor causes dramatic axon guidance and branching deficits, leading to a loss of geniculate neurons. To determine whether the developmental functions of p75 in geniculate neurons are cell autonomous, we deleted p75 specifically in Phox2b + oral sensory neurons (Phox2b-Cre; p75fx/fx) or in neural crest-derived cells (P0-Cre; p75fx/fx) and examined geniculate neuron development. In germline p75−/− mice half of all geniculate neurons were lost. The proportion of Phox2b + neurons, as compared to Phox2b-pinna-projecting neurons, was not altered, indicating that both populations were affected similarly. Chorda tympani nerve recordings demonstrated that p75−/− mice exhibit profound deficits in responses to taste and tactile stimuli. In contrast to p75−/− mice, there was no loss of geniculate neurons in either Phox2b-Cre; p75fx/fx or P0-Cre; p75fx/fx mice. Electrophysiological analyses demonstrated that Phox2b-Cre; p75fx/fx mice had normal taste and oral tactile responses. There was a modest but significant loss of fungiform taste buds in Phox2b-Cre; p75fx/fx mice, although there was not a loss of chemosensory innervation of the remaining fungiform taste buds. Overall, these data suggest that the developmental functions of p75 are largely cell non-autonomous and require p75 expression in other cell types of the chorda tympani circuit.

357 Early life factors shaping gut development and lifelong disease risk

Abstract The first 3–4 months of postnatal life represents a critical period in gastrointestinal (GI) development that shapes lifelong function and disease resistance. During this period, extensive maturation of the immune and nervous systems, and epithelial transport and barrier function, occurs. While some aspects of early life gut development are genetically “hard-wired,” the GI system exhibits a high degree of plasticity, and thus developmental trajectory and long-term function can be significantly modified during this period via host and environmental influences. Stress or adversity during early critical periods of development has been recognized as a significant risk factor for the later-life susceptibility to several GI and systemic chronic inflammatory and debilitating diseases in humans and animals, including functional bowel disorders characterized by dysmotility and neuroinflammation, but also disease associated with systemic inflammation, such as metabolic disorders (obesity and Type 2 diabetes) and neurobehavioral disorders including anxiety and depression. Moreover, early life stressors include routine management practices such as maternal separation and early weaning, social disruption, and early immune activation from disease or vaccination, and thus early life stress is common in animals. While the link between early life adversity and later life disease risk is well-established across species, the mechanisms that link early life stress, gut development and lifelong disease risk are poorly understood, and thus targeted management, therapeutic and nutritional strategies to reduce the negative impacts of early life stress are lacking. This goal of this presentation is to provide a biological framework for understanding how early life environmental and host factors such as stress and biological sex can alter the normal trajectory of GI development and disease risk throughout the lifespan. Ways in which changes in gut development might drive the risk for diseases important to many species, such as metabolic disease, functional/inflammatory bowel disorders and neurobehavioral disorders, will be discussed.

Inhibition of progesterone receptor activity during development increases reelin-immunoreactivity in Cajal-Retzius cells, alters synaptic innervation in neonatal dentate gyrus, and impairs episodic-like memory in adulthood

Progesterone receptor (PR) is expressed in Cajal-Retzius (CR) cells of the dentate gyrus (DG) molecular layer during the postnatal period (P1–28), a critical stage of development for the dentate gyrus and its circuitry. CR cells secrete the glycoprotein, reelin, which is required for typical development of the DG and its connections, particularly afferent input from the perforant path. This pathway regulates the processing of sensory information arriving from entorhinal cortex and integrates this information to form episodic memories. To assess the potential role of PR activity on the development of these connections and associated behavior, rats were treated daily from P1 to 7 with the PR antagonist, RU486. RU486 treatment increased the number of reelin-ir cells, suggesting an accumulation of reelin, and implicating PR in the regulation of a principle developmental function of CR cells. RU486 also altered the synaptic bouton marker, synaptophysin-ir, in a sex-specific manner, suggesting a role for PR activity in the development of perforant path innervation of the molecular layer (MOL). Finally, both control and RU486 treated rats spent significantly more time with a temporally distant object in the Relative Recency task, suggesting an intact associative memory for object identity and temporal order in both groups. In contrast, the same RU486 treated rats were impaired in an episodic-like memory task compared to controls, failing to integrate object identity (‘what’), time (‘when’), and object position (‘where’). These findings reveal a novel role for PR in regulating CR cell function within the MOL, thereby altering development of DG connectivity and behavioral function.

Facilitation of Bone Healing Processes Based on the Developmental Function of Meox2 in Tooth Loss Lesion.

In the present study, we examined the bone healing capacity of Meox2, a homeobox gene that plays essential roles in the differentiation of a range of developing tissues, and identified its putative function in palatogenesis. We applied the knocking down of Meox2 in human periodontal ligament fibroblasts to examine the osteogenic potential of Meox2. Additionally, we applied in vivo periodontitis induced experiment to reveal the possible application of Meox2 knockdown for 1 and 2 weeks in bone healing processes. We examined the detailed histomorphological changes using Masson’s trichrome staining and micro-computed tomography evaluation. Moreover, we observed the localization patterns of various signaling molecules, including α-SMA, CK14, IL-1β, and MPO to examine the altered bone healing processes. Furthermore, we investigated the process of bone formation using immunohistochemistry of Osteocalcin and Runx2. On the basis of the results, we suggest that the knocking down of Meox2 via the activation of osteoblast and modulation of inflammation would be a plausible answer for bone regeneration as a gene therapy. Additionally, we propose that the purpose-dependent selection and application of developmental regulation genes are important for the functional regeneration of specific tissues and organs, where the pathological condition of tooth loss lesion would be.

Developmental Roles of FUSE Binding Protein 1 (Fubp1) in Tooth Morphogenesis.

FUSE binding protein 1 (Fubp1), a regulator of the c-Myc transcription factor and a DNA/RNA-binding protein, plays important roles in the regulation of gene transcription and cellular physiology. In this study, to reveal the precise developmental function of Fubp1, we examined the detailed expression pattern and developmental function of Fubp1 during tooth morphogenesis by RT-qPCR, in situ hybridization, and knock-down study using in vitro organ cultivation methods. In embryogenesis, Fubp1 is obviously expressed in the enamel organ and condensed mesenchyme, known to be important for proper tooth formation. Knocking down Fubp1 at E14 for two days, showed the altered expression patterns of tooth development related signalling molecules, including Bmps and Fgf4. In addition, transient knock-down of Fubp1 at E14 revealed changes in the localization patterns of c-Myc and cell proliferation in epithelium and mesenchyme, related with altered tooth morphogenesis. These results also showed the decreased amelogenin and dentin sialophosphoprotein expressions and disrupted enamel rod and interrod formation in one- and three-week renal transplanted teeth respectively. Thus, our results suggested that Fubp1 plays a modulating role during dentinogenesis and amelogenesis by regulating the expression pattern of signalling molecules to achieve the proper structural formation of hard tissue matrices and crown morphogenesis in mice molar development.

Hippocampal and cortical tissue-specific epigenetic clocks indicate an increased epigenetic age in a mouse model for Alzheimer's disease.

Epigenetic clocks are based on age-associated changes in DNA methylation of CpG-sites, which can accurately measure chronological age in different species. Recently, several studies have indicated that the difference between chronological and epigenetic age, defined as the age acceleration, could reflect biological age indicating functional decline and age-associated diseases. In humans, an epigenetic clock associated Alzheimer’s disease (AD) pathology with an acceleration of the epigenetic age. In this study, we developed and validated two mouse brain region-specific epigenetic clocks from the C57BL/6J hippocampus and cerebral cortex. Both clocks, which could successfully estimate chronological age, were further validated in a widely used mouse model for AD, the triple transgenic AD (3xTg-AD) mouse. We observed an epigenetic age acceleration indicating an increased biological age for the 3xTg-AD mice compared to non-pathological C57BL/6J mice, which was more pronounced in the cortex as compared to the hippocampus. Genomic region enrichment analysis revealed that age-dependent CpGs were enriched in genes related to developmental, aging-related, neuronal and neurodegenerative functions. Due to the limited access of human brain tissues, these epigenetic clocks specific for mouse cortex and hippocampus might be important in further unravelling the role of epigenetic mechanisms underlying AD pathology or brain aging in general.

Oι θετικές ψευδαισθήσεις για τον εαυτό και η ριψοκίνδυνη συμπεριφορά στην εφηβεία: Ανασκόπηση της βιβλιογραφίας

The objective of this study is, through the relevant literature review, to point out the associations between risk-taking behavior during adolescence and positive illusions about the self, that is imaginary audience and personal fable ideations. Positive illusions about the self and risky behavior in adolescence are usually investigated as a direct result of adolescent egocentrism. in this study we briefly describe the main theoretical approaches of positive illusions about the self. Moreover, research findings are presented on the mediating role of self-esteem in the relationship between positive illusions about the self (mainly personal fable) and risk-taking in adolescence. also, we discuss age and gender effects on the complex phenomenon of risk-taking and we focus on adaptive developmental functions of positive illusions about the self. in particular, we focus on the dual function of the personal fable ideation: the illusions of omnipotence and invulnerability either lead adolescents and young adults to risk-taking, or they contribute both to a positive self-image projection in the future and to individuals’ functional adaptation to new situations in their transition from adolescence to adulthood.

In vivo light-sheet microscopy resolves localisation patterns of FSD1, a superoxide dismutase with function in root development and osmoprotection.

Superoxide dismutases (SODs) are enzymes detoxifying superoxide to hydrogen peroxide while temporal developmental expression and subcellular localisation are linked to their functions. Therefore, we aimed here to reveal in vivo developmental expression, subcellular, tissue- and organ-specific localisation of iron superoxide dismutase 1 (FSD1) in Arabidopsis using light-sheet and Airyscan confocal microscopy. FSD1-GFP temporarily accumulated at the site of endosperm rupture during seed germination. In emerged roots, it showed the highest abundance in cells of the lateral root cap, columella, and endodermis/cortex initials. The largest subcellular pool of FSD1-GFP was localised in the plastid stroma, while it was also located in the nuclei and cytosol. The majority of the nuclear FSD1-GFP is immobile as revealed by fluorescence recovery after photobleaching. We found that fsd1 knockout mutants exhibit reduced lateral root number and this phenotype was reverted by genetic complementation. Mutant analysis also revealed a requirement for FSD1 in seed germination during salt stress. Salt stress tolerance was coupled with the accumulation of FSD1-GFP in Hechtian strands and superoxide removal. It is likely that the plastidic pool is required for acquiring oxidative stress tolerance in Arabidopsis. This study suggests new developmental and osmoprotective functions of SODs in plants.

Notch Signaling and Liver Cancer.

Interactions between liver cells are closely regulated by Notch signaling. Notch signaling has been reported clinically related to bile duct hypogenesis in Alagille syndrome, which is caused by mutations in the Jagged1 gene. Notch activation and hepatocarcinogenesis are closely associated since cancer signaling is affected by the development of liver cells and cancer stem cells. Gene expression and genomic analysis using a microarray revealed that abnormalities in Notch-related genes were associated with the aggressiveness of liver cancer. This pattern was also accompanied with α-fetoprotein- and EpCAM-expressing phenotypes in vitro, in vivo, and in clinical tissues. Hepatitis B or C virus chronic infection or alcohol- or steatosis-related liver fibrosis induces liver cancer. Previous reports demonstrated that HBx, a hepatitis B virus protein, was associated with Jagged1 expression. We found that the Jagged1 and Notch1 signaling pathways were closely associated with the transcription of covalently closed circular hepatitis B virus DNA, which regulated cAMP response element-binding protein, thereby affecting Notch1 regulation by the E3 ubiquitin ligase ITCH. This viral pathogenesis in hepatocytes induces liver cancer. In conclusion, Notch signaling exerts various actions and is a clinical signature associated with hepatocarcinogenesis and liver context-related developmental function.

Concepts and functions of small RNA pathways in C. elegans.

A diversity of gene regulatory mechanisms drives the changes in gene expression required for animal development. Here, we discuss the developmental roles of a class of gene regulatory factors composed of a core protein subunit of the Argonaute family and a 21-26-nucleotide RNA cofactor. These represent ancient regulatory complexes, originally evolved to repress genomic parasites such as transposons, viruses and retroviruses. However, over the course of evolution, small RNA-guided pathways have expanded and diversified, and they play multiple roles across all eukaryotes. Pertinent to this review, Argonaute and small RNA-mediated regulation has acquired numerous functions that affect all aspects of animal life. The regulatory function is provided by the Argonaute protein and its interactors, while the small RNA provides target specificity, guiding the Argonaute to a complementary RNA. C. elegans has 19 different, functional Argonautes, defining distinct yet interconnected pathways. Each Argonaute binds a relatively well-defined class of small RNA with distinct molecular properties. A broad classification of animal small RNA pathways distinguishes between two groups: (i) the microRNA pathway is involved in repressing relatively specific endogenous genes and (ii) the other small RNA pathways, which effectively act as a genomic immune system to primarily repress expression of foreign or "non-self" RNA while maintaining correct endogenous gene expression. microRNAs play prominent direct roles in all developmental stages, adult physiology and lifespan. The other small RNA pathways act primarily in the germline, but their impact extends far beyond, into embryogenesis and adult physiology, and even to subsequent generations. Here, we review the mechanisms and developmental functions of the diverse small RNA pathways of C. elegans.

First person – Éva Saskői

ABSTRACTFirst Person is a series of interviews with the first authors of a selection of papers published in Disease Models & Mechanisms, helping early-career researchers promote themselves alongside their papers. Éva Saskői is first author on ‘The SDHB Arg230His mutation causing familial paraganglioma alters glycolysis in a new Caenorhabditis elegans model’, published in DMM. Éva is a PhD student in the lab of Krisztina Takács-Vellai at Eötvös Lorand University, Budapest, Hungary, investigating the developmental functions of tumor suppressor homologs in Caenorhabditis elegans.

Developmentally-programmed cellular senescence is conserved and widespread in zebrafish.

Cellular senescence is considered a stress response imposing a stable cell cycle arrest to restrict the growth of damaged cells. More recently however, cellular senescence was identified during mouse embryo development at particular structures during specific periods of time. This programmed cell senescence has been proposed to serve developmental and morphogenetic functions and to potentially represent an evolutionary origin of senescence. Cellular senescence has also been described to take place during bird (chick and quail) and amphibian (xenopus and axoltl) development. Fish however, have been described to show a very narrow and restricted pattern of developmental cell senescence. Here we carried out a detailed characterization of senescence during zebrafish development and found it to be conserved and widespread. Apart from yolk and cloaca, previously described structures, we also identified senescence in the developing central nervous system, intestine, liver, pronephric ducts, and crystalline. Interestingly, senescence at these developing structures disappeared upon treatment with senolytic compound ABT-263, supporting their senescent identity and opening the possibility of studying the contribution of this process to development. In summary, our findings extend the description of developmentally-programmed cell senescence to lower vertebrates contributing to the notion of the relevance of this process for embryo development.

CAPt'n of Actin Dynamics: Recent Advances in the Molecular, Developmental and Physiological Functions of Cyclase-Associated Protein (CAP).

Cyclase-associated protein (CAP) has been discovered three decades ago in budding yeast as a protein that associates with the cyclic adenosine monophosphate (cAMP)-producing adenylyl cyclase and that suppresses a hyperactive RAS2 variant. Since that time, CAP has been identified in all eukaryotic species examined and it became evident that the activity in RAS-cAMP signaling is restricted to a limited number of species. Instead, its actin binding activity is conserved among eukaryotes and actin cytoskeleton regulation emerged as its primary function. However, for many years, the molecular functions as well as the developmental and physiological relevance of CAP remained unknown. In the present article, we will compile important recent progress on its molecular functions that identified CAP as a novel key regulator of actin dynamics, i.e., the spatiotemporally controlled assembly and disassembly of actin filaments (F-actin). These studies unraveled a cooperation with ADF/Cofilin and Twinfilin in F-actin disassembly, a nucleotide exchange activity on globular actin monomers (G-actin) that is required for F-actin assembly and an inhibitory function towards the F-actin assembly factor INF2. Moreover, by focusing on selected model organisms, we will review current literature on its developmental and physiological functions, and we will present studies implicating CAP in human pathologies. Together, this review article summarizes and discusses recent achievements in understanding the molecular, developmental and physiological functions of CAP, which led this protein emerge as a novel CAPt’n of actin dynamics.

AMP1 and CYP78A5/7 act through a common pathway to govern cell fate maintenance in Arabidopsis thaliana.

Higher plants can continuously form new organs by the sustained activity of pluripotent stem cells. These stem cells are embedded in meristems, where they produce descendants, which undergo cell proliferation and differentiation programs in a spatiotemporally-controlled manner. Under certain conditions, pluripotency can be reestablished in descending cells and this reversion in cell fate appears to be actively suppressed by the existing stem cell pool. Mutation of the putative carboxypeptidase ALTERED MERISTEM PROGRAM1 (AMP1) in Arabidopsis causes defects in the suppression of pluripotency in cells normally programmed for differentiation, giving rise to unique hypertrophic phenotypes during embryogenesis as well as in the shoot apical meristem. A role of AMP1 in the miRNA-dependent control of translation has recently been established, however, how this activity is connected to its developmental functions is not resolved. Here we identify members of the cytochrome P450 clade CYP78A to act in parallel with AMP1 to control cell fate in Arabidopsis. Mutation of CYP78A5 and its close homolog CYP78A7 in a cyp78a5,7 double mutant caused suspensor-to-embryo conversion and ectopic stem cell pool formation in the shoot meristem, phenotypes characteristic for amp1. The tissues affected in the mutants showed pronounced expression levels of AMP1 and CYP78A5 in wild type. A comparison of mutant transcriptomic responses revealed an intriguing degree of overlap and highlighted alterations in protein lipidation processes. Moreover, we also found elevated protein levels of selected miRNA targets in cyp78a5,7. Based on comprehensive genetic interaction studies we propose a model in which both enzyme classes act on a common downstream process to sustain cell fate decisions in the early embryo and the shoot apical meristem.

Structural Models for the Dynamic Effects of Loss-of-Function Variants in the Human SIM1 Protein Transcriptional Activation Domain

Single-minded homologue 1 (SIM1) is a transcription factor with numerous different physiological and developmental functions. SIM1 is a member of the class I basic helix-loop-helix-PER-ARNT-SIM (bHLH–PAS) transcription factor family, that includes several other conserved proteins, including the hypoxia-inducible factors, aryl hydrocarbon receptor, neuronal PAS proteins, and the CLOCK circadian regulator. Recent studies of HIF-a-ARNT and CLOCK-BMAL1 protein complexes have revealed the organization of their bHLH, PASA, and PASB domains and provided insight into how these heterodimeric protein complexes form; however, experimental structures for SIM1 have been lacking. Here, we describe the first full-length atomic structural model for human SIM1 with its binding partner ARNT in a heterodimeric complex and analyze several pathogenic variants utilizing state-of-the-art simulations and algorithms. Using local and global positional deviation metrics, deductions to the structural basis for the individual mutants are addressed in terms of the deleterious structural reorganizations that could alter protein function. We propose new experiments to probe these hypotheses and examine an interesting SIM1 dynamic behavior. The conformational dynamics demonstrates conformational changes on local and global regions that represent a mechanism for dysfunction in variants presented. In addition, we used our ab initio hybrid model for further prediction of variant hotspots that can be engineered to test for counter variant (restoration of wild-type function) or basic research probe.

The implementation of resilience based clinical supervision to support transition to practice in newly qualified healthcare professionals

BackgroundHealthcare workforce shortages are an international issue. This service development targets the contributory element of poor retention amongst newly qualified nurses. Resilience Based Clinical Supervision is underpinned by the principles of Compassion Focused Therapy. It aims to alleviate work related stress and support individuals to reframe their experiences through structured and reflective discussion. It incorporates skills which develop proficiency in mindfulness, distress tolerance and positive reframing. ObjectivesTo explore the acceptability, feasibility, and experience of Resilience Based Clinical Supervision to support transition to practice in newly qualified nurses. DesignAn extensive program of champion (N = 40) and cascade (N = 78) training for facilitators was implemented as a development of their standard transition to practice package. SettingsSix pilot sites within the UK. ParticipantsNewly qualified nurses (266) received a minimum of six Resilience Based Clinical Supervision sessions over a one-year period. MethodsData were gathered via eleven focus groups (n = 48). A deductive and collaborative approach to content analysis was utilised to consider the perceived outcomes, challenges, experience and best practice amongst both facilitators and nurses' transitioning from student to registered practitioner. ResultsAnalysis showed the new registrants were extending and accepting compassion to and from their peers, signifying the compassionate flow within the group setting. This was continued through the development of self-care strategies utilised in practice, which allowed compassion to flow into patient care and towards colleagues. ConclusionsThe main perceived outcome of RBCS was recognised as restorative. However, the growth of skills for self-care, emotional intelligence, and confidence to challenge poor working conditions also indicated a developmental function. These perceived outcomes have the potential to result in positive implications for workforce retention. Importantly, findings draw attention to the importance of wider organisational commitment and structures which support and respond to RBCS facilitator and participant concerns.

Developmental Modulation of Root Cell Wall Architecture Confers Resistance to an Oomycete Pathogen

SummaryThe cell wall is the primary interface between plant cells and their immediate environment and must balance multiple functionalities, including the regulation of growth, the entry of beneficial microbes, and protection against pathogens. Here, we demonstrate how API, a SCAR2 protein component of the SCAR/WAVE complex, controls the root cell wall architecture important for pathogenic oomycete and symbiotic bacterial interactions in legumes. A mutation in API results in root resistance to the pathogen Phytophthora palmivora and colonization defects by symbiotic rhizobia. Although api mutant plants do not exhibit significant overall growth and development defects, their root cells display delayed actin and endomembrane trafficking dynamics and selectively secrete less of the cell wall polysaccharide xyloglucan. Changes associated with a loss of API establish a cell wall architecture with altered biochemical properties that hinder P. palmivora infection progress. Thus, developmental stage-dependent modifications of the cell wall, driven by SCAR/WAVE, are important in balancing cell wall developmental functions and microbial invasion.