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Sorrentino, N. C.

Publications and source records attributed to Sorrentino, N. C..

2 recordsLinked to original sources

De novo Golgi biogenesis requires coordinated transactivation of a Golgi regulon

The Golgi apparatus expands during differentiation and high secretory demand, yet the transcriptional control of its biogenesis remains poorly defined. Here, we developed a targeted enzymatic ablation method to eliminate the Golgi and trigger de novo organelle formation. Single-cell RNA-seq of cells rebuilding Golgi revealed an orchestrated induction of a broad Golgi gene network coinciding with structural and functional organelle maturation. This gene set spans all Golgi sub-compartments and functions, including glycosylation, trafficking, and ion transport, thus supporting the concept of a unified Golgi regulon, enabling the simultaneous expression of components required for the organelle structural and functional integrity. Through promoter analysis and RNAi screening, we identified CREB3L1 as a key transcriptional regulator critical for Golgi gene activation and organelle reformation. These findings indicate that CREB3L1-dependent transcriptional mechanisms orchestrate a complete Golgi biogenesis program that may be essential for organelle regeneration and for secretory pathway plasticity during physiological remodeling.

cell biology↗

Role of trafficking protein particle complex 2 in medaka development

The skeletal dysplasia spondyloepiphyseal dysplasia tarda (SEDT) is caused by mutations in the TRAPPC2 gene, which encodes Sedlin, a component of the trafficking protein particle (TRAPP) complex that we have shown previously to be required for the export of type II collagen (Col2) from the endoplasmic reticulum. No vertebrate model for SEDT has been generated thus far. To address this gap, we generated a Sedlin knockout animal by mutating the orthologous TRAPPC2 gene (olSedl) of Oryzias latipes (medaka) fish. OlSedl deficiency leads to embryonic defects, short size, diminished skeletal ossification, and altered Col2 production and secretion, resembling human defects observed in SEDT patients. Moreover, SEDT knock-out animals display photoreceptor degeneration and gut morphogenesis defects, suggesting a key role for Sedlin in the development of these organs. Thus, by studying Sedlin function in vivo, we provide evidence for a mechanistic link between TRAPPC2-mediated membrane trafficking, Col2 export, and developmental disorders.

cell biology↗