The hairy–downy game revisited: an empirical test of the interspecific social dominance mimicry hypothesis

© 2018 The Association for the Study of Animal Behaviour. Understanding the emergence and persistence of convergent phenotypes is the subject of considerable debate. Species may converge on nearly identical phenotypes for a variety of reasons, including occupying similar environments, exhibiting similar foraging ecologies, and for signalling reasons such as mimicry. Interspecific social dominance mimicry (ISDM) is a hypothesis that states that socially subordinate species evolve a phenotype mimicking a dominant species so as to accrue resources and avoid aggression. A recently proposed test case for this phenomenon asserts that downy woodpeckers, Picoides pubescens, evolved mimetic plumage to avoid attacks from hairy woodpeckers, Picoides villosus. We examined this claim with a large behavioural data set collected by citizen scientists. We employed phylogenetic methods and simulations to test whether downy woodpeckers avoid aggression, and whether downy woodpeckers are more dominant than expected based on body mass. Contrary to the expectations of ISDM, we found that downy woodpeckers were markedly more often the target of hairy woodpecker attacks than expected based on their relative abundances. Our empirical data thus offers no support for the strict ISDM hypothesis as an explanation for downy–hairy woodpecker plumage convergence. However, downy woodpeckers are slightly more dominant than expected based on their body mass, albeit not significantly so. Our data therefore lend weight to previous suggestions that the benefits of mimicry potentially accrue from third-party species mistaking the mimic for the model, rather than the model mistaking the mimic for another model

Molecular heterogeneity in pediatric malignant rhabdoid tumors in patients with multi-organ involvement

Rhabdoid tumors (RTs) of the brain (atypical teratoid/rhabdoid tumor; AT/RT) and extracranial sites (most often the kidney; RTK) are malignant tumors predominantly occurring in children, frequently those wit

A fluid biomarker reveals loss of TDP-43 splicing repression in presymptomatic ALS-FTD

Although loss of TAR DNA-binding protein 43 kDa (TDP-43) splicing repression is well documented in postmortem tissues of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), whether this abnormality occurs during early-stage disease remains unresolved. Cryptic exon inclusion reflects loss of function of TDP-43, and thus detection of proteins containing cryptic exon-encoded neoepitopes in cerebrospinal fluid (CSF) or blood could reveal the earliest stages of TDP-43 dysregulation in patients. Here we use a newly characterized monoclonal antibody specific to a TDP-43-dependent cryptic epitope (encoded by the cryptic exon found in HDGFL2) to show that loss of TDP-43 splicing repression occurs in ALS-FTD, including in presymptomatic C9orf72 mutation carriers. Cryptic hepatoma-derived growth factor-like protein 2 (HDGFL2) accumulates in CSF at significantly higher levels in familial ALS-FTD and sporadic ALS compared with controls and is elevated earlier than neurofilament light and phosphorylated neurofilament heavy chain protein levels in familial disease. Cryptic HDGFL2 can also be detected in blood of individuals with ALS-FTD, including in presymptomatic C9orf72 mutation carriers, and accumulates at levels highly correlated with those in CSF. Our findings indicate that loss of TDP-43 cryptic splicing repression occurs early in disease progression, even presymptomatically, and that detection of the HDGFL2 cryptic neoepitope serves as a potential diagnostic biomarker for ALS, which should facilitate patient recruitment and measurement of target engagement in clinical trials