Stem cell-derived retinal organoids are a useful tool to understand the pathobiology of devastating retinal degenerations and can aid to identify and validate therapeutics to promote rescue.

Chimeric RNAs are widely distributed spatiotemporally during human retinal development and have important regulatory functions, such as silencing of CTNNBIP1-CLSTN1 biasing the progenitor cells toward the RPE cell fate at the expense of neural retinal cell fates.

The integrated analysis of multi-omics and functional evidence both in vitro and in knock-in mouse models reveal novel gain-of-function pathogenic mechanisms of dominant CRX HD missense mutations.

Study of human, knockout mice, and in-vitro models revealed CEP78 absence is the genetical cause of cone-rod dystrophy and male infertility with multiple morphological abnormalities of sperm flagella, CEP78 interacted with IFT20 and TTC21A to modulate cilliogenesis and centriole length.

NMNAT1, a ubiquitously expressed metabolic enzyme linked to inherited blinding disease, is crucial for the proper differentiation of photoreceptor cells and subsequent survival of multiple cell types in the retina.

Silencers and enhancers targeted by a common transcription factor in photoreceptors are distinguished by the number and diversity of binding transcription factor binding sites they contain.

A mouse model of retinal degeneration reveals a common mechanism for axonal degeneration and photoreceptor cell death and identifies SARM1 as a therapeutic candidate for retinopathies.

A data-driven within-host model reveals that different antibiotics are associated with divergent effects on antibiotic resistance carriage and abundance in hospitalised patients, with important implications for antibiotic stewardship.