these same skeletal lineages reproduces key features of diabetic fracture healing. Together, these findings point to a novel FOXO1-primary cilia axis as a central regulator of skeletal repair in diabetes.
The successful candidate will investigate how diabetes-driven FOXO1 activity suppresses ciliogenesis and regenerative signaling in chondrocytes and osteoblasts. The project will use conditional mouse models targeting FOXO1, IFT80, and combined FOXO1/IFT80 deletion; diabetic fracture models; spatial transcriptomics; single-cell RNA sequencing; histology; immunostaining; microCT; and biomechanical testing.
A major translational component will test a newly developed nanofiber hydrogel carrying an IGF-1 mimetic, NFH-IGF, designed for controlled local release at the fracture site. The goal is to determine whether NFH-IGF can restore cilia-dependent signaling, suppress FOXO1 activity, and improve fracture healing in type 1 and type 2 diabetes.
Qualifications
Applicants should have a PhD, MD, DMD, DVM, or equivalent degree in skeletal biology, cell biology, molecular biology, bioengineering, diabetes biology, immunology, or a related field. Experience with mouse models, bone or cartilage biology, fracture healing, imaging, molecular assays, spatial transcriptomics, single-cell RNAseq, or bioinformatics is desirable.
Application Instructions
This position offers an opportunity to work at the interface of skeletal biology, diabetes complications, primary cilia signaling, regenerative biomaterials, and high-dimensional genomics, with strong potential for high-impact mechanistic and translational discoveries.
To apply, send a cover letter, CV, and contact information for three references and submit through interfolio.
