Author Correction: Myeloid lineage enhancers drive oncogene synergy in CEBPA/CSF3R mutant acute myeloid leukemia

Signal transducer and activator of transcription (STAT) proteins act downstream of cytokine receptors to facilitate changes in gene expression that impact a range of developmental and homeostatic processes. Patients harbouring loss-of-function (LOF) STAT5B mutations exhibit postnatal growth failure due to lack of responsiveness to growth hormone as well as immune perturbation, a disorder called growth hormone insensitivity syndrome with immune dysregulation 1 (GHISID1). This study aimed to generate a zebrafish model of this disease by targeting the stat5.1 gene using CRISPR/Cas9 and characterising the effects on growth and immunity. The zebrafish Stat5.1 mutants were smaller, but exhibited increased adiposity, with concomitant dysregulation of growth and lipid metabolism genes. The mutants also displayed impaired lymphopoiesis with reduced T cells throughout the lifespan, along with broader disruption of the lymphoid compartment in adulthood, including evidence of T cell activation. Collectively, these findings confirm that zebrafish Stat5.1 mutants mimic the clinical impacts of human STAT5B LOF mutations, establishing them as a model of GHISID1.

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A zebrafish model of growth hormone insensitivity syndrome with immune dysregulation 1 (GHISID1)

Heidary

Awasthi

Page

et al. 2023

Cell. Mol. Life Sci.

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Author Correction: Myeloid lineage enhancers drive oncogene synergy in CEBPA/CSF3R mutant acute myeloid leukemia

Abstract: Since the publication of this work, Brittany M. Curtiss has changed their name from Brittany M. Smith. This has now been amended.

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A zebrafish model of growth hormone insensitivity syndrome with immune dysregulation 1 (GHISID1)

A zebrafish model of growth hormone insensitivity syndrome with immune dysregulation 1 (GHISID1)

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