journal article
LitStream Collection
Home
Goloe, Daniel; Gildor, Tsvia; Ben‐Tabou de‐Leon, Smadar
2024 Genesis: The Journal of Genetics and Development
doi: 10.1002/dvg.23614pmid: 39139086
Organisms from the five kingdoms of life use minerals to harden their tissues and make teeth, shells and skeletons, in the process of biomineralization. The sea urchin larval skeleton is an excellent system to study the biological regulation of biomineralization and its evolution. The gene regulatory network (GRN) that controls sea urchin skeletogenesis is known in great details and shows similarity to the GRN that controls vertebrates' vascularization while it is quite distinct from the GRN that drives vertebrates' bone formation. Yet, transforming growth factor beta (TGF‐β) signaling regulates both sea urchin and vertebrates' skeletogenesis. Here, we study the upstream regulation and identify transcriptional targets of TGF‐β in the Mediterranean Sea urchin species, Paracentrotus lividus. TGF‐βRII is transiently active in the skeletogenic cells downstream of vascular endothelial growth factor (VEGF) signaling, in P. lividus. Continuous perturbation of TGF‐βRII activity significantly impairs skeletal elongation and the expression of key skeletogenic genes. Perturbation of TGF‐βRII after skeletal initiation leads to a delay in skeletal elongation and minor changes in gene expression. TGF‐β targets are distinct from its transcriptional targets during vertebrates' bone formation, suggesting that the role of TGF‐β in biomineralization in these two phyla results from convergent evolution.
Damuth, Dillon L.; Cunningham, Doreen D.; Silva, Elena M.
2024 Genesis: The Journal of Genetics and Development
doi: 10.1002/dvg.23612pmid: 39054872
The SRY HMG box transcription factor Sox21 plays multiple critical roles in neurogenesis, with its function dependent on concentration and developmental stage. In the allotetraploid Xenopus laevis, there are two homeologs of sox21, namely sox21.S and sox21.L. Previous studies focused on Sox21.S, but its amino acid sequence is divergent, lacking conserved poly‐A stretches and bearing more similarity with ancestral homologs. In contrast, Sox21.L shares higher sequence similarity with mouse and chick Sox21. To determine if Sox21.S and Sox21.L have distinct functions, we conducted gain and loss‐of‐function studies in Xenopus embryos. Our studies revealed that Sox21.S and Sox21.L are functionally redundant, but Sox21.L is more effective at driving changes than Sox21.S. These results also support our earlier findings in ectodermal explants, demonstrating that Sox21 function is dose‐dependent. While Sox21 is necessary for primary neuron formation, high levels prevent their formation. Strikingly, these proteins autoregulate, with high levels of Sox21.L reducing sox21.S and sox21.L mRNA levels, and decreased Sox21.S promoting increased expression of sox21.L. Our findings shed light on the intricate concentration‐dependent roles of Sox21 homeologs in Xenopus neurogenesis.
Bright, Cora L.; Bomze, Howard M.; Bhaumik, Mantu; Kay, Jeremy N.; Cartoni, Romain; Gospe, Sidney M.
2024 Genesis: The Journal of Genetics and Development
doi: 10.1002/dvg.23615pmid: 39139090
Armadillo repeat‐containing X‐linked protein‐1 (Armcx1) is a poorly characterized transmembrane protein that regulates mitochondrial transport in neurons. Its overexpression has been shown to induce neurite outgrowth in embryonic neurons and to promote retinal ganglion cell (RGC) survival and axonal regrowth in a mouse optic nerve crush model. In order to evaluate the functions of endogenous Armcx1 in vivo, we have created a conditional Armcx1 knockout mouse line in which the entire coding region of the Armcx1 gene is flanked by loxP sites. This Armcx1fl line was crossed with mouse strains in which Cre recombinase expression is driven by the promoters for β‐actin and Six3, in order to achieve deletion of Armcx1 globally and in retinal neurons, respectively. Having confirmed deletion of the gene, we proceeded to characterize the abundance and morphology of RGCs in Armcx1 knockout mice aged to 15 months. Under normal physiological conditions, no evidence of aberrant retinal or optic nerve development or RGC degeneration was observed in these mice. The Armcx1fl mouse should be valuable for future studies investigating mitochondrial morphology and transport in the absence of Armcx1 and in determining the susceptibility of Armcx1‐deficient neurons to degeneration in the setting of additional heritable or environmental stressors.
Showing 1 to 5 of 5 Articles