Integrating decades of small-scale experiments with human gene expression data provides a systems-level view of the coordinated molecular processes triggered by spinal cord injury, and their relationship to recovery.
PRDM13, a transcriptional repressor, antagonizes activity of basic-helix-loop-helix transcriptional activators and protects the developing spinal cord from aberrant expression of ventral-restricted cell-type regulators to generate the correct composition of neurons in the dorsal spinal cord.
The complex chromatin-based genomic regulatory system controlling developmental gene expression in complex bilaterians predates the evolution of morphological complexity and may have been a prerequisite for the evolution of the first simple multicellular animals.
The MYC transcription factor network member MGA is a subunit of a non-canonical Polycomb complex, which, when inactivated, accelerates tumorigenesis in mouse models of cancer and proliferation in colon organoids.
Quantitative analyses associating the morphology of developing organs with dynamic gene expression patterns can reveal biological phenomena that cause malformations and malfunction but remain elusive to traditional qualitative assessments.