Erosive hand osteoarthritis (EHOA) is a chronic joint disease characterized by severe inflammation and degeneration of cartilage and bone tissue. As this disease is multifactorial in nature, the molecular mechanisms that influence its pathogenesis are unclear, leading to a lack of disease-modifying therapies. However, by screening 40 families with a dominant inheritance pattern for EHOA, we identified two independent germline heterozygous mutations that associated with EHOA onset: PANX1 [c.G455A:p.R152H] and PANX3 [c.G71A:p.R24H]. Pannexin 1 (PANX1) and Pannexin 3 (PANX3) are mechanosensitive channel-forming glycoproteins that pass various metabolites and ions such as adenosine triphosphate (ATP) and calcium to regulate numerous physiological and cellular processes including tissue development, cell differentiation, and homeostasis. In this study, we report that electrophysiological recordings, ATP release, and basal dye uptake assays revealed increased channel activity of the PANX1 R152H variant, which led to increased cytotoxicity following long-term expression. In contrast, R24H mutant PANX3 channels exhibited a loss-of-function in mechanically stimulated dye uptake assays. Under stable, moderate expression conditions, this reduction in channel activity was associated with decreased cell growth, whereas overexpression led to increased cell death. In vivo, R24H expression in zebrafish embryos increased apoptosis and upregulation of p21 and osteogenic genes. Together these findings demonstrate that two mutations with opposing alterations in PANX channel activity, hyperactivity in R152H PANX1 and loss-of-function in R24H PANX3, can converge on degenerative cellular outcomes. Collectively, we report the first germline PANX3 mutation associated with disease and provide the first evidence linking PANX1 and PANX3 mutations to human erosive osteoarthritis.

Glioblastoma (GBM) is the most common primary brain tumour, with a median survival of 12-18 months, highlighting a need for new treatment targets. We observed that pannexin 1 (PANX1), a channel-forming glycoprotein important in purinergic signalling, is upregulated in GBM compared to normal tissue and expressed throughout patient tumours. Western blot analysis of patient-derived GBM cell lines revealed significantly increased PANX1 expression in these primary lines compared to brain tissue and control glial cells. Bulk RNA-sequencing compared the gene expression of GBM cells devoid of PANX1 via CRISPR/Cas9 deletion (PANX1-KO) compared to controls. Gene Ontology and KEGG gene set analyses revealed PANX1-KO in GBM cells affects cell surface and cell junction components, processes, and pathways, including the HIPPO pathway, in addition to critically downregulating β-catenin mRNA and other components of the Wnt pathway. The deletion of PANX1 resulted in a disruption of the β-catenin protein and a dramatic reduction in migration and cell growth. Pharmacological inhibition of PANX1 in GBM cells with Probenecid (PBN) and Spironolactone (SPIR) demonstrated a significant reduction in live cell numbers and migration via scratch assay. Both blockers dramatically decreased F-actin filament formation, and the cellular localization of beta-catenin became more intracellular compared to controls. Xenografted GBM tumours showed a reduction in tumour cell viability by bioluminescent imaging and reduced hemorrhaging incidence when treated with PBN. These new insights support further investigation of PANX1 as a potential GBM therapeutic target and its role in multiple cancer signaling pathways that regulate this devastating disease.

Here we characterize seven Cx30.3 gene variants (R22H, S26Y, P61R, C86S, E99K, T130M and M190L) clinically associated with the rare skin disorder erythrokeratodermia variabilis et progressiva (EKVP) in tissue-relevant and differentiation-competent rat epidermal keratinocytes (REKs). We found that all variants, when expressed alone or together with wildtype (WT) Cx30.3, had the capacity to traffic and form gap junctions with an efficiency like WT Cx30.3. Cx30.3 was found to have a slower relative turnover than Cx43. However, turnover was more rapid for the R22H and P61R variants relative to Cx30.3. Furthermore, REKs that expressed the P61R variant exhibited reduced viability and were more permeable to fluorescent dyes, indicative of leaky hemichannels and/or the loss of membrane integrity associated with cell death. In connexin-null AD-293 cells, dual patch clamp studies revealed that the variants had either reduced (C86S) or no (S26Y and T130M) gap junction channel function. The remaining variants formed functional gap junction channels with enhanced transjunctional voltage (Vj)-dependent gating. Moreover, WT Cx30.3 and functional variant gap junction channels had similar unitary conductance of ∼34-42 pS, though variant channels appeared to have lower open probability than WT Cx30.3 channels at high Vjs. In conclusion, EKVP-associated Cx30.3 variants each alter one or more Cx30.3 characteristics although the molecular changes identified for E99K were limited to enhanced Vj gating. The breadth of molecular changes identified may all be sufficient to cause EKVP, but this remains to be firmly established as more familial patients are genotyped for these variants. KEY POINTS: Here we characterize seven Cx30.3 variants (R22H, S26Y, P61R, C86S, E99K, T130M and M190L) that have been clinically associated with the rare skin disorder erythrokeratodermia variabilis et progressiva (EKVP). We discovered human Cx30.3 undergoes relatively slow turnover compared with Cx43 and exhibits kinetically slow and limited voltage gating. Wildtype Cx30.3 and all variants localized to intracellular compartments and gap junctions in rat epidermal keratinocytes. Each EKVP-associated Cx30.3 variant altered one or more Cx30.3 characteristics related to protein stability, cell viability and/or channel function. The breadth of molecular changes identified for each Cx30.3 variant may independently be sufficient to cause EKVP, but this remains to be firmly established through additional genetic and molecular analysis.

In this study, we explored the intricate relationship between Pannexin 1 (PANX1) and the Hippo signaling pathway effector, Yes-associated protein (YAP). Analysis of The Cancer Genome Atlas (TCGA) data revealed a significant positive correlation between PANX1 mRNA and core Hippo components, Yes-associated protein 1 [YAP], Transcriptional coactivator with PDZ-binding motif [TAZ], and Hippo scaffold, Ras GTPase-activating-like protein IQGAP1 [IQGAP1], in invasive cutaneous melanoma and breast carcinoma. Furthermore, we demonstrated that PANX1 expression is upregulated in invasive melanoma cell lines and is associated with increased YAP protein levels. Notably, our investigations uncovered a previously unrecognized interaction between endogenous PANX1 and the Hippo scaffold protein IQGAP1 in melanoma cells. Moreover, our findings revealed that IQGAP1 exhibits differential expression in melanoma cells and plays a regulatory role in cellular morphology. Functional studies involving PANX1 knockdown provided compelling evidence that PANX1 modulates YAP protein levels and its cotranscriptional activity in melanoma and breast carcinoma cells. Importantly, our study highlights the potential therapeutic significance of targeting PANX1. Pharmacological inhibition of PANX1 using selective FDA-approved inhibitors or PANX1 knockdown reduced YAP levels in melanoma cells. Furthermore, our Clariom™ S analysis unveiled key genes implicated in cell proliferation, such as neuroglin1 (NRG1), β-galactoside binding protein and galectin-3 (LGALS3), that are affected in PANX1-deficient cells. In summary, our investigation delves into the intricate interplay between PANX1 and YAP in the context of invasive melanoma, offering valuable insights into potential therapeutic strategies for effective treatment.

Pannexin 1 (PANX1) is upregulated in many cancers, where its channel activity and signalling promote tumorigenic properties. Here, we report that potential internal translation start sites exist in mouse and human PANX1 which have implications in trafficking and protein interaction. Using mouse PANX1 constructs for each internal methionine (M) we saw that the shorter PANX1 isoforms were glycosylated, able to traffic to the cell surface and PANX1-M37 formed channels which could be activated by C-terminus cleavage or α1-adrenoceptor stimulation. Furthermore, we report a novel ∼25 kDa isoform of human PANX1 (hPANX1-25K) which lacks the N-terminus and was detected in several human cancer cell lines including melanoma, osteosarcoma, breast cancer, and glioblastoma multiforme. This isoform was increased upon hPANX1 CRISPR/Cas9 deletion targeting the first exon near M1, and using Expasy PeptideCutter we did not find any evidence of hPANX1 cleavage sites which would produce a 25 kDa fragment, suggesting a potential alternative translation initiation site as the source of hPANX1-25K. hPANX1-25K was confirmed to be a hPANX1 isoform via mass spectrometry, can be N-linked glycosylated at multiple sites including the canonical N255 and novel N338 and N394 residues, and can interact with both β-catenin and full length hPANX1. Using cell surface biotinylation and immunocytochemistry, we also determined hPANX1-25K exhibits a predominantly intracellular localization. hPANX1-25K is prevalent throughout melanoma progression, and its levels are increased in squamous cell carcinoma cells and patient-derived tumours, compared to keratinocytes and patient-matched normal skin, indicating that it may be differentially regulated in normal and cancer cells.

Pannexin (PANX) channels are present in skin and facilitate the movement of signalling molecules during cellular communication. PANX1 and PANX3 function in skin homeostasis and keratinocyte differentiation but were previously reduced in a small cohort of human cutaneous squamous cell carcinoma (cSCC) tumours compared to normal epidermis. In our study we used SCC-13 cells, limited publicly available RNA-seq data and a larger cohort of cSCC patient-matched samples to analyse PANX1 and PANX3 expression and determine the association between their dysregulation and the malignant properties of cSCC. In a bioinformatics analysis, PANX1 transcripts were increased in cSCC and head and neck SCC tumours compared to normal tissues, but PANX3 mRNA showed no differences. However, in our own cohort PANX3 transcripts were decreased in cSCC compared to patient-matched aged skin, whereas PANX1 protein was upregulated in cSCC. PANX1 localized to all regions within the cSCC tumour microenvironment, and increased levels were associated with larger tumour dimensions. To investigate PANX1 function in SCC-13 cells, we deleted PANX1 via CRISPR/Cas9 and treated with PANX1 inhibitors, which markedly reduced cell growth and migration. To assess PANX3 function in cutaneous carcinogenesis, we employed the 7,12-dimethylbenz(a)anthracene/12-otetradecanoylphorbol-13-acetate (DMBA/TPA) model using our global Panx3 knockout (KO) mice, where 60% of wild-type and 100% of KO mice formed precancerous papillomas. Average papilloma volumes at endpoint were significantly increased in KO mice and showed moderate evidence of increases in KO mice over time. Collectively, these findings suggest PANX1 and PANX3 dysregulation may have potential tumour-promoting and tumour-suppressive effects for keratinocyte transformation, respectively. KEY POINTS: Pannexin 1 (PANX1) and pannexin 3 (PANX3) are channel-forming proteins which are critical in the normal maintenance and function of keratinocytes in the skin but may become altered in cutaneous squamous cell carcinoma (cSCC) tumours. In this study we used a combination of culture models, mouse models and patient-derived tissues. We found PANX1 levels are increased in cSCC tumours and present in all tumour regions, functioning to promote cSCC cell growth and migration. Conversely, PANX3 levels are decreased in cSCC tumours, and this protein reduces the incidence and growth of precancerous lesions. Taken together our data indicate that in cSCC these pannexin family members seem to have opposite effects, in either promoting or restricting cancer cell properties. These results help us to better understand the mechanisms of malignant transformation of keratinocytes and offer a new potential therapeutic target for the treatment of advanced cSCC.

Responsible and sustainable fisheries management requires a comprehensive knowledge of stock structure. Here, we examine population structure in the blue-swimmer crab (Portunus armatus), which supports one of the largest commercial and recreational fisheries within Western Australia (WA). Tissue samples from adult P. armatus were collected from 16 sites along the WA coastline from Albany to the Kimberley, a distance spanning over 3000 km. Adult individuals were also collected from one site in South Australia (SA) and one in the Northern Territory (NT), the latter separated into two morphologically similar species, P. armatus and P. pelagicus, as their ranges are known to overlap in northern Australia. Juvenile crabs were also sampled from five sites within the south-west region of WA to test for evidence of local recruitment. Using a panel of 11,175 single-nucleotide polymorphism (SNP) loci, we found evidence of two genetically distinct clusters in the NT sample and the northernmost WA site in the Kimberley region consistent with two sympatric species. We also found evidence of hybridisation between the two groups where they co-occur. Subsequent analyses on the remaining WA sites and SA, revealed the presence of four genetically distinct populations, represented by sites at SA, Exmouth, Shark Bay and the south-west region of WA. Additional analyses focussing on the south-west of WA exclusively failed to detect any appreciable population structure within this region. Consistent with this pattern, juveniles collected from five sites within south-west region of WA were no more genetically related to other juveniles from the same sampling site, on average, than juveniles collected elsewhere. Our results suggest the south-west region of WA is comprised of a single panmictic population, consistent with the view that populations along this coastline are highly interconnected due to inshore and offshore currents. Future management should consider a more integrated approach for managing blue-swimmer crab fisheries within the south west region of WA and improved monitoring in northern Australia, where two genetically distinct groups are currently fished as a single stock.

Connexins are channel-forming proteins that function to facilitate gap junctional intercellular communication. Here, we use dual cell voltage clamp and dye transfer studies to corroborate past findings showing that Cx31.1 (encoded by GJB5) is defective in gap junction channel formation, illustrating that Cx31.1 alone does not form functional gap junction channels in connexin-deficient mammalian cells. Rather Cx31.1 transiently localizes to the secretory pathway with a subpopulation reaching the cell surface, which is rarely seen in puncta reminiscent of gap junctions. Intracellular retained Cx31.1 was subject to degradation as Cx31.1 accumulated in the presence of proteasomal inhibition, had a faster turnover when Cx43 was present and ultimately reached lysosomes. Although intracellularly retained Cx31.1 was found to interact with Cx43, this interaction did not rescue its delivery to the cell surface. Conversely, the co-expression of Cx31 dramatically rescued the assembly of Cx31.1 into gap junctions where gap junction-mediated dye transfer was enhanced. Collectively, our results indicate that the localization and functional status of Cx31.1 is altered through selective interplay with coexpressed connexins, perhaps suggesting Cx31.1 is a key regulator of intercellular signaling in keratinocytes.

Immunotherapies for malignant melanoma seek to boost the anti‐tumoral response of CD8 + T cells, but have a limited patient response rate, in part due to limited tumoral immune cell infiltration. Genetic or pharmacological inhibition of the pannexin 1 (PANX1) channel‐forming protein is known to decrease melanoma cell tumorigenic properties in vitro and ex vivo . Here, we crossed Panx1 knockout ( Panx1 −/− ) mice with the inducible melanoma model Braf CA , Pten loxP , Tyr::CreER T2 (BPC). We found that deleting the Panx1 gene in mice does not reduce BRAF(V600E)/Pten‐driven primary tumor formation or improve survival. However, tumors in BPC‐ Panx1 −/− mice exhibited a significant increase in the infiltration of CD8 + T lymphocytes, with no changes in the expression of early T‐cell activation marker CD69, lymphocyte activation gene 3 protein (LAG‐3) checkpoint receptor, or programmed cell death ligand‐1 (PD‐L1) in tumors when compared to the BPC‐ Panx1 +/+ genotype. Our results suggest that, although Panx1 deletion does not overturn the aggressive BRAF / Pten ‐driven melanoma progression in vivo , it does increase the infiltration of effector immune T‐cell populations in the tumor microenvironment. We propose that PANX1‐targeted therapy could be explored as a strategy to increase tumor‐infiltrating lymphocytes to boost anti‐tumor immunity.

The channel-forming glycoprotein PANX3 functions in cutaneous wound healing and keratinocyte differentiation, but its role in maintaining skin homeostasis through aging is not yet understood. We found that PANX3 is absent in newborn skin but becomes upregulated with age. We characterized the skin of global Panx3-knockout (KO) mice and found that KO dorsal skin showed sex differences at different ages but generally had reduced dermal and hypodermal areas compared with age-matched controls. Transcriptomic analysis of the KO epidermis revealed reduced E-cadherin stabilization and Wnt signaling compared with that of wild-type, consistent with the inability of primary KO keratinocytes to adhere in culture and diminished epidermal barrier function in KO mice. We also observed increased inflammatory signaling in the KO epidermis and a higher incidence of dermatitis in aged KO mice compared with that in wild-type controls. These findings suggest that during skin aging, PANX3 is critical in the maintenance of dorsal skin architecture, keratinocyte cell-cell and cell-matrix adhesion, and inflammatory skin responses.

Blue swimmer crab species are widely distributed in Indian and west Pacific Oceans including the coastline around Australia and have been identified as potential candidates for stock enhancement. A recent taxonomic review revealed the presence of two blue swimmer crab species in Australia, namely Portunus armatus which is found around most of the Australian coastline, and Portunus pelagicus which is found in the northern coast where it is sympatric with P. armatus. It is important to understand population structure and genetic diversity of Portunus spp. to efficiently manage stocks. In the present study we investigated species classification and population structure of Portunus spp. in Australia using full and partial genomic information, namely mitochondrial COX1 gene sequences derived from whole genome sequencing and single nucleotide polymorphic (SNP) markers developed from partial genome sequencing. Blue swimmer crab samples were collected from the western (n = 52), northern (n = 17) and eastern (n = 110) coasts of Australia. Genetic diversity and population genetic structure were assessed for within and between region variation. Our genomic results indicated the presence of two blue swimmer crab species in Australia. One, namely, P. pelagicus was found only in Northern Territory (Darwin), and other, namely P. armatus was found around Australia. There was evidence of natural hybridisation between two species in Northern Territory (Darwin) where they were sympatric. P. armatus populations from the western, northern and eastern regions were genetically different although there were no significant genetic differences observed between the Queensland and New South Wales populations nor between the two neighbouring populations in Western Australia. Results found in the present study supports the view that the P. armatus populations in western, northern and eastern regions of Australia should be treated as at least three different stocks. A lack of genetic structuring along the eastern coast suggests blue swimmer crabs can be considered as a single stock along the sampled range at least in relation to fisheries enhancement, release programs and broodstock management.

Epidermal keratinocytes are enriched with at least nine connexins that are key regulators of epidermal homeostasis. The role of Cx30.3 in keratinocytes and epidermal health became evident when fourteen autosomal dominant mutations in the Cx30.3-encoding GJB4 gene were linked to a rare and incurable skin disorder called erythrokeratodermia variabilis et progressiva (EKVP). While these variants are linked to EKVP, they remain largely uncharacterized hindering therapeutic options. In this study, we characterize the expression and functional status of three EKVP-linked Cx30.3 mutants (G12D, T85P, and F189Y) in tissue-relevant and differentiation-competent rat epidermal keratinocytes. We found that GFP-tagged Cx30.3 mutants were non-functional likely due to their impaired trafficking and primary entrapment within the endoplasmic reticulum (ER). However, all mutants failed to increase BiP/GRP78 levels suggesting they were not inducing an unfolded protein response. FLAG-tagged Cx30.3 mutants were also trafficking impaired yet occasionally exhibited some capacity to assemble into gap junctions. The pathological impact of these mutants may extend beyond their trafficking deficiencies as keratinocytes expressing FLAG-tagged Cx30.3 mutants exhibited increased propidium iodide uptake in the absence of divalent cations. Attempts to rescue the delivery of trafficking impaired GFP-tagged Cx30.3 mutants into gap junctions by chemical chaperone treatment were ineffective. However, co-expression of wild type Cx30.3 greatly enhanced the assembly of Cx30.3 mutants into gap junctions, although endogenous levels of Cx30.3 do not appear to prevent the skin pathology found in patients harboring these autosomal dominant mutations. In addition, a spectrum of connexin isoforms (Cx26, Cx30, and Cx43) exhibited the differential ability to trans-dominantly rescue the assembly of GFP-tagged Cx30.3 mutants into gap junctions suggesting a broad range of connexins found in keratinocytes may favourably interact with Cx30.3 mutants. We conclude that selective upregulation of compatible wild type connexins in keratinocytes may have potential therapeutic value in rescuing epidermal defects invoked by Cx30.3 EKVP-linked mutants.

Brain metastases are the most common central nervous system malignancy, and the leading cause of cancer-related deaths. Non-small cell lung carcinomas (NSCLC) comprise the most common cell of origin. Immunotherapy, particularly checkpoint inhibitors, has emerged as the standard of care for many patients with advanced lung cancer. Pannexin1 (PANX1) is a transmembrane glycoprotein that forms large-pore channels and has been reported to promote cancer metastasis. However, the roles of PANX1 in lung cancer brain metastases and tumor immune microenvironment have not been characterized. 42 patient-matched formalin-fixed paraffin-embedded tissue samples from lung carcinomas and the subsequent brain metastases were constructed into three tissue microarrays (TMAs). PANX1 and markers of tumor-infiltrating immune cells (CD3, CD4, CD8, CD68, and TMEM119) were assessed using immunohistochemistry and digital image analysis. The expression of PANX1 was significantly higher in brain metastases than in their paired primary lung carcinoma. The high levels of PANX1 in lung carcinoma cells in the brain inversely correlated with infiltration of peripheral blood-derived macrophages. Our findings highlight the role of PANX1 in the progression of metastatic NSCLC, and the potential therapeutic approach of targeting PANX1 enhances the efficacy of immune checkpoint inhibitors in brain metastasis.

Pannexins (PANX) are a family of three channel-forming membrane glycoproteins expressed in the skin. Previous studies have focused on the role of PANX1 and PANX3 in the regulation of cellular functions in skin cells while PANX2, the largest member of this protein family, has not been investigated. In the current study, we explored the temporal PANX2 expression in murine skin and found that one Panx2 splice variant (Panx2-202) tends to be more abundant at the protein level and is continuously expressed in developed skin. PANX2 was detected in the suprabasal layers of the mouse epidermis and up-regulated in an in vitro model of rat epidermal keratinocyte differentiation. Furthermore, we show that in apoptotic rat keratinocytes, upon UV light B (UVB)-induced caspase-3/7 activation, ectopically overexpressed PANX2 is cleaved in its C-terminal domain at the D416 residue without increasing the apoptotic rate measured by caspase-3/7 activation. Notably, CRISPR-Cas9 mediated genetic deletion of rat Panx2 delays but does not impair caspase-3/7 activation and cytotoxicity in UVB-irradiated keratinocytes. We propose that endogenous PANX2 expression in keratinocytes promotes cell death after UVB insult and may contribute to skin homeostasis.

The channel-forming glycoprotein Pannexin 3 (PANX3) functions in cutaneous wound healing and keratinocyte differentiation, but its role in skin homeostasis through aging is not yet understood. We found that PANX3 is absent in newborn skin but becomes upregulated with age. We characterized the skin of global Panx3 knockout mice (KO) and found that KO dorsal skin showed sex-differences at different ages, but generally had reduced dermal and hypodermal areas compared to aged-matched controls. Transcriptomic analysis of KO epidermis revealed reduced E-cadherin stabilization and Wnt signalling compared to WT, consistent with the inability of primary KO keratinocytes to adhere in culture, and diminished epidermal barrier function in KO mice. We also observed increased inflammatory signalling in KO epidermis and higher incidence of dermatitis in aged KO mice compared to wildtype controls. These findings suggest that during skin aging, PANX3 is critical in the maintenance of dorsal skin architecture, keratinocyte cell-cell and cell-matrix adhesion and inflammatory skin responses.

The potential of microvascular ultrasound techniques for detecting anti-angiogenic treatment response in cancer models is widely recognized. This study assesses the usefulness of the perfusion parameters from SVD-based optimal shrinkage clutter filtered power Doppler (PD) and statistical histogram-based contrast-enhanced ultrasound (CEUS) images, compared to perfusion parameters from conventional PD and mean-intensity-based CEUS images, in improving the antiangiogenic tumor treatment response classification of cell lines with differing sensitivity level. Eleven perfusion parameters and the tumor volume feature are fed into a multivariable logistic regression learning model to classify antiangiogenic treatment responses of renal cell carcinoma cell lines, Caki-1 (very sensitive) and ACHN (resistant), engrafted on a chicken embryo assay. Results indicated that the model with selected parameters from statistical CEUS analysis, SVD-filtered 2D PD images outperformed a model using all microvascular features and a classifier with features from conventional analysis of CEUS and PD only. Therefore, the perfusion parameters from SVD-based PD and statistical CEUS method are best used as a supplement to conventional PD and CEUS analysis.

There are several ways to set biological reference points (BRP) for harvest strategies, but one of the most direct methods is to use the stock-recruitment relationship (SRR). Even if the SRR is not statistically significant, it provides valuable information about the spawning stock levels that don't influence the recruitment that is relevant to setting BRP. Environmental factors, particularly extreme events such as the 2011 Western Australia (WA) marine heatwave, are typically a major driver of recruitment, so it is important to assess their influence as ignoring this effect may bias the SRR. This study examines the SRR for 13 invertebrate stocks in WA including lobster, prawn, scallop, abalone, pearl oysters and crabs. These stocks have long time series of fishery-independent juvenile abundance indices, which provide a clear signal of the year-class strength that improves the ability to assess the SRR and environmental effects. Eleven stocks showed a significant environmental effect on recruitment with seven stocks demonstrating a significant spawning stock effect. The stock-recruitment data is used to determine the BRP based on the species' specific biological information, even when the relationship is not significant. Importantly, management action in the harvest control rules is not just reactive to low spawning stock levels but is proactive based on the juvenile abundance to ensure that the level of fishing results in future spawning stocks being maintained above the BRP. This evidence-based approach to setting BRPs and the proactive management approach adopted in the harvest strategy can be invaluable to fisheries management generally.

While many global fisheries rely on commercial catch and effort statistics to inform stock assessments and management, alternative approaches are required for small-scale recreational fisheries. In this study, a citizen science program was implemented to collect recreational catch and effort and fishery-independent data using three Western Australian blue swimmer crab (Portunus armatus) fisheries as case studies. Between 2013 and 2019, an opt-in Research Angler Program (RAP) was supported by 102 diarists submitting data from 1,705 fishing events, with direct and regular contact proving important for maintaining participation. Representing the only current recreational crabbing information for the three fisheries, the RAP data proved valuable in assessing management options (e.g. increases in size limits, bag limit reductions, seasonal closures) during a recent review of the Western Australian P. armatus resource. Two follow-up surveys to canvass diarist attitudes towards the program identified a desire to contribute to research and management, and concerns about fish stocks, as key motivations for involvement. In addition, 26 diarists assisted with fishery-independent breeding stock surveys (FIS) to collect valuable stock assessment data. The RAP and FIS proved complementary, as the first provided useful spatial/temporal coverage of catch rates and catch composition, while the second gave a targeted assessment of breeding stock abundance. We demonstrate how the data can generate annual fishery performance indices, such as standardised recreational catch rates and a fishery-independent egg production index, to support a potential harvest strategy. This study highlights a cost-effective and highly valuable citizen science approach to obtain key information for the assessment and management of small scale recreational fisheries, with suggested recommendations for researchers considering a similar approach elsewhere.

Identification of key drivers of population dynamics and prediction of rates of population recovery following stock decline are crucial aspects of fisheries management. The abundance of a blue swimmer crab population (Portunus armatus) in Cockburn Sound, Western Australia, which once supported the largest commercial fishery for this short-lived species in the State, declined markedly and has remained low despite two commercial fishery closures. This study employed state-space biomass dynamics models to explore evidence for potential factors contributing to the lack of stock recovery, including fishing pressure, changes in primary production (using chlorophyll-a as a proxy) and depensatory stock-recruitment dynamics. Likelihood ratio test results indicated better statistical fits for models with production functions modified to account for chlorophyll-a or both depensation and chlorophyll-a. Models incorporating both depensation and chlorophyll-a provided the most biologically-feasible results (e.g. estimated intrinsic increase, r, not near zero) and the estimated biomass trajectories were less uncertain. For all models, estimated annual harvest rates peaked in the late 1990s, prior to the first major stock decline, and again in 2009−12, when the fishery was briefly re-opened with tight management restrictions. Results for models including both depensation and chlorophyll-a indicated that stock productivity is positively-related to chlorophyll-a. Thus, below-average chlorophyll-a concentrations in Cockburn Sound in recent years, in combination with some form(s) of depensation (e.g. associated with predation pressure), may be preventing stock recovery. Despite a sustained period of very limited recreational fishing and no commercial fishing, stock recovery appears highly uncertain under current environmental conditions. The results of this study highlight the value of incorporating environmental data and alternative stock-recruitment assumptions when fitting production models to explore key factors influencing population dynamics.