The human Fibrodysplasia-Ossificans-Progressiva BMP-receptor mutant signals in zebrafish in the absence of ligand-binding, displays BMP ligand-responsive hyperactivity, neither requiring other type-I-BMP receptors, unlike wild-type, challenging views of the pathological mechanism.

Disrupted mesenchymal Bmpr1a-mediated signaling in fetal mouse lung leads to abnormal airway development and congenital pulmonary cyst formation.

Members of the BMP family of growth factors act as a reiterative code of distinct activities to direct the identities of different classes of sensory neurons in the spinal cord.

Hepatic stellate cells play a central role in maintaining liver health by mediating cell-to-cell crosstalk via the production of GDF2 and BMP10.

Multivariate genotype-phenotype mapping enables quantification of pathway and process-level effects on complex phenotypes and predicts phenotypic effects of novel mutations.

Uncovering a new function of BMP signaling and enhancing our comprehension of the pathogenesis of microtia.

Clonal heterozygosity for recessive disease alleles can elicit unexpected phenotypes in vivo, suggesting a new genetic concept relevant to understanding pathogenesis (deleterious heteromosaicism).

Key functional variants, discovered using Massively Parallel Reporter Assay (MPRA) and reporter assays in the context of SARS-CoV-2 infection, support the importance of two critical chemokine receptor genes CCR1 and CCR5 in severe Covid-19 illness.

A neural precursor cell defect precedes widespread inflammation, amyloid plaque pathology, and cognitive deficit in Alzheimer's disease, which can be reversed by inhibiting USP16.

The non-signaling complex formed by Activin A and ACVR1 is operant in vivo and is required to temper the degree of heterotopic ossification in the genetic disorder fibrodysplasia ossificans progressiva.