Biology subjects

Song, J. L.

Publications and source records attributed to Song, J. L..

3 recordsLinked to original sources

bioRxiv2022

RNA localization to the mitotic spindle regulated by kinesin-1 and dynein is essential for early development of the sea urchin embryo

Mitosis is a fundamental and highly regulated process that acts to faithfully segregate chromosomes into two identical daughter cells. Transcript localization of genes involved in mitosis to the mitotic spindle may be an evolutionarily conserved mechanism to ensure that mitosis occurs in a timely manner. We identified many RNA transcripts that encode proteins involved in mitosis localized at the mitotic spindles in dividing sea urchin embryos and mammalian cells. Disruption of microtubule polymerization, kinesin-1, or dynein results in lack of spindle localization of these transcripts in the sea urchin embryo. Further, results indicate that the cytoplasmic polyadenylation element (CPE) within the 3UTR of Aurora B, a recognition sequence of CPEB, is essential for RNA localization to the mitotic spindle. Blocking this sequence results in arrested development during early cleavage stages, suggesting that RNA localization to the mitotic spindle may be a regulatory mechanism of cell division that is important for early development.

cell biology↗

bioRxiv2022

microRNA-1 represses signaling pathway components to impact embryonic structures derived from all three germ layers

microRNAs are evolutionarily conserved non-coding RNAs that direct post-transcriptional regulation of target transcripts. We use the sea urchin embryo to achieve a comprehensive understanding of miR-1s function in a developing embryo. Results indicate that miR-1 regulates gut contractions, specification, and positioning of serotonergic neurons, as well as mesodermally-derived muscles, pigment cells, and skeletogenic cells. Gain-of-function of miR-1 generally leads to more severe developmental defects than its loss-of-function. We identified that miR-1 directly suppresses Ets1/2, Tbr, and VegfR7 of the skeletogenic gene regulatory network, and Notch, Nodal, and Wnt1 signaling components. We found that miR-1s direct suppression of Nodal may indirectly regulate FoxQ2 to impact serotonergic neurons. Excess miR-1 may lead to decreased Nodal and Notch that result in decreased circumpharnygeal muscle fibers and the number of pigment cells. The striking ectopic skeletal branching induced by miR-1 mimic injections may be explained by miR-1s direct suppression of Nodal that leads to expression changes of Vegf3, and Fgfa that mediate skeletogenesis. This work demonstrates that miR-1 plays a diverse regulatory role that impacts tissues derived from all germ layers. Summary statementThis study identifies wide-ranging regulatory roles and regulatory mechanisms of miR-1 that impact structures derived from all three germ layers during embryonic development.

developmental biology↗

bioRxiv2021

miR-124 regulates Notch and NeuroD1 to mediate transition states of neuronal development

MicroRNAs (miRNAs) regulate gene expression by destabilizing target mRNA and/or inhibiting translation in animal cells. The ability to mechanistically dissect the function of miR-124 during specification, differentiation, and maturation of neurons during development within a single system has not been accomplished. Using the sea urchin (Strongylocentrotus purpuratus) embryo, we take advantage of the manipulability of the embryo and its well-documented gene regulatory networks (GRNs). We incorporated NeuroD1 as part of the sea urchin neuronal GRN and determined that miR-124 inhibition resulted in decreased gut contractions, swimming velocity, and neuronal development. We further integrated post-transcriptional regulation of miR-124 into the neuronal GRN. Inhibition of miR-124 resulted in increased number of cells expressing transcription factors associated with progenitor neurons and a concurrent decrease of mature and functional neurons. Results revealed that miR-124 regulates undefined factors early in neurogenesis during neuronal specification and differentiation in the early blastula and gastrula stages. In the late gastrula and larval stages, miR-124 regulates Notch and NeuroD1. Specifically, miR-124 regulates the transition between neuronal differentiation and maturation, by directly suppressing NeuroD1. Removal of miR-124s suppression of NeuroD1 results in increased mature neurons with decreased Synaptagmin B-positive mature, functional neurons. By removing both miR-124 suppression of NeuroD1 and Notch, we were able to phenocopy miR-124 inhibitor induced defects. Overall, we have improved the neuronal GRN and identified miR-124 to play a prolific role in regulating various transitions of neuronal development.

neuroscience↗