UNC-16 interacts with LRK-1 and WDFY-3 to regulate the termination of axon growth.

In humans, MAPK8IP3 (also known as JIP3) is a neurodevelopmental disorder-associated gene. In Caenorhabditis elegans, the UNC-16 ortholog of the MAPK8IP3 protein can regulate the termination of axon growth. However, its role in this process is not well understood.

UNC-16 interacts with LRK-1 and WDFY-3 to regulate the termination of axon growth.

is a neurodevelopmental-disorder associated gene that can regulate the termination of axon growth. However, its role in this process is not well understood. Here, we report that UNC-16 promotes axon termination through a process that includes the LRK-1(LRRK-1/LRRK-2) kinase and the WDFY-3 (WDFY3/Alfy) selective autophagy protein.

Autism candidate gene () regulates MALS-1 to protect against mitochondrial dysfunction and axon degeneration during neurodevelopment.

Mitochondrial dysfunction is thought to be a key component of neurodevelopmental disorders such as autism, intellectual disability, and ADHD. However, little is known about the molecular mechanisms that protect against mitochondrial dysfunction during neurodevelopment. Here, we address this question through the investigation of , the ortholog of the autism candidate gene, which encodes an RNA-binding protein whose role in neurons is unknown.

The ANC-1 (Nesprin-1/2) organelle-anchoring protein functions through mitochondria to polarize axon growth in response to SLT-1.

A family of giant KASH proteins, including C. elegans ANC-1 and mammalian Nesprin-1 and -2, are involved in organelle anchoring and are associated with multiple neurodevelopmental disorders including autism, bipolar disorder, and schizophrenia. However, little is known about how these proteins function in neurons.

Lessons learned from a lncRNA odyssey for two genes with vascular functions, DLL4 and TIE1.

Pervasive transcription is a feature of the human genome that requires better understanding. Over the last decade or so, RNA species longer than 200 nucleotides-dubbed long non-coding RNA (lncRNAs)-had been found in sense or anti-sense orientation within or outside of genes that encode proteins. Importantly, lncRNA-mediated gene regulation and the elements that control lncRNA expression are a source of fascination among molecular biologists.

Temporal and Spatial Post-Transcriptional Regulation of Zebrafish mRNA by Long Noncoding RNA During Brain Vascular Assembly.

Objective: Tie1 (tyrosine kinase containing immunoglobulin and epidermal growth factor homology 1), an endothelial and hematopoietic cell-specific receptor tyrosine kinase, is an important regulator of angiogenesis and critical for maintaining vascular integrity. The post-transcriptional regulation of mRNA expression is not understood, but it might partly explain Tie1's differential expression pattern in endothelium. Following up on our previous work that identified natural antisense transcripts from the locus- (), which regulates mRNA levels in zebrafish-we attempted to identify the mechanism of this regulation.

Mechanisms of translational repression of the Smcp mRNA in round spermatids.

The protamine 1 (Prm1) and sperm mitochondria-associated, cysteine-rich protein (Smcp) mRNAs exemplify a widespread pattern of mRNA-specific regulation of mRNA translation in post-meiotic spermatogenic cells, spermatids. Both mRNAs are transcribed and initially stored in free-mRNPs in early spermatids, and translated on polysomes in late spermatids. In this study, we demonstrate that the 5' and 3'-UTRs and the 3' terminus of the Smcp 3'-UTR are required for normal repression of the Smcp mRNA in transgenic mice.

Identification of elements in the Smcp 5' and 3' UTR that repress translation and promote the formation of heavy inactive mRNPs in spermatids by analysis of mutations in transgenic mice.

The sperm mitochondria-associated cysteine-rich protein (Smcp) mRNA is transcribed in step 3 spermatids, and is stored in free mRNPs until translation begins ∼6 days later in step 11. To identify sequences that control the timing of Smcp mRNA translation, mutations in both UTRs were analyzed in transgenic mice using green fluorescent protein (GFP), squashes of seminiferous tubules, and quantification of polysomal loading in adult and 21 dpp testes in sucrose and Nycodenz gradients. GFP fluorescence is first detected in step 9 spermatids in lines harboring a transgene containing the Gfp 5' UTR and Smcp 3' UTR.