Practical Resources for Talking to Children with Autism about Systemic Racism.

As part of the child-rearing process, situations that invite difficult conversations will inevitably arise. Oftentimes, there are no guidelines or structure for how to discuss topics such as sex education, systemic racism, bullying, grieving, and gun violence. Accordingly, adults may feel at a loss for how to address difficult topics and may even avoid difficult conversations completely. When adults choose to have these conversations, they may imitate the conversations their caregivers had with them, and therefore further the cycle of systemic racism, often unknowingly and unintentionally. Racial injustice has been a core part of the American experience since the founding of the republic; hence, conversations about systemic racism are long overdue. The need has significantly increased, given the current socio-political climate. Social justice may be a sensitive topic for some, but it is a needed conversation for all, including children with Autism Spectrum Disorder (ASD). Currently available curricula and teaching manuals in the Applied Behavior Analysis (ABA) literature include little or no resources for caregivers on how to address systemic racism with their children on the spectrum. Children with ASD should be educated about how they, and their families, can combat systemic racism in their everyday lives. The present paper addresses this gap in available treatment resources by offering practical suggestions and guidelines for how adults can address the topic of systemic racism with children on the autism spectrum to educate them and prepare them to contribute to a more equitable and just future.

TGFß signalling acts as a molecular brake of myoblast fusion.

Fusion of nascent myoblasts to pre-existing myofibres is critical for skeletal muscle growth and repair. The vast majority of molecules known to regulate myoblast fusion are necessary in this process. Here, we uncover, through high-throughput in vitro assays and in vivo studies in the chicken embryo, that TGFß (SMAD2/3-dependent) signalling acts specifically and uniquely as a molecular brake on muscle fusion. While constitutive activation of the pathway arrests fusion, its inhibition leads to a striking over-fusion phenotype. This dynamic control of TGFß signalling in the embryonic muscle relies on a receptor complementation mechanism, prompted by the merging of myoblasts with myofibres, each carrying one component of the heterodimer receptor complex. The competence of myofibres to fuse is likely restored through endocytic degradation of activated receptors. Altogether, this study shows that muscle fusion relies on TGFß signalling to regulate its pace.