bioRxiv Science⌕ Search

Biology subjects

Martin, S. B.

Publications and source records attributed to Martin, S. B..

2 recordsLinked to original sources

Single cell sequencing during the entire life cycle reveals cell type diversity in Oikopleura dioica, and pools of genes expressed in the house-producing epithelium

In tunicates, larvaceans represent a fascinating case of evolution, where the chordate body plan has been maintained despite a rapidly evolving genome characterized by strong In contrast to other tunicates, larvaceans keep the chordate body plan during their entire life. They have acquired a highly specialized epithelium in charge of producing the "house", a complex extracellular apparatus used for filter feeding in the plankton. To what extent the house and this epithelium represent true molecular innovations withing chordates is a question for which thorough transcriptomics can bring novel insights. We conducted a developmental profiling of gene expression at the single-cell level in the larvacean Oikopleura dioica. We provide detailed descriptions of cellular transcriptomes associated with the house-synthesizing organ, which permits to define the molecular specifics of epithelial cell territories. We followed their emergence during development, and we identified genes that represent key candidate molecules for regulating the morphogenesis of the house-producing organ. Dynamic changes in gene expression and cell identities during major developmental transitions of the lifecycle illustrate that our dataset effectively allows access to the diversity of O. dioicas cell types in embryos and in adults. The resources presented here constitute critical assets to investigate larvacean biology and evolution for mechanistic and comparative goals.

evolutionary biology↗

Nodal/Smad2 signaling sustains developmental pausing by repressing Pparg-mediated lipid metabolism

Cells and organisms can enter transient dormant states to survive unfavorable conditions during development, physiological adult contexts, and disease. One paradigmatic case of dormancy is diapause, whereby embryos transiently pause development and enter a state of suspended animation. In mammals, diapause occurs pre-implantation at the blastocyst state and involves global growth suppression and metabolic rewiring towards lipid usage as energy source. The molecular regulation of diapause remains poorly understood, including whether it occurs by default or requires active signaling. Here, we identify the Transforming Growth Factor-beta (TGF-{beta}) signaling pathway as an essential driver of transcriptional and metabolic reprogramming in diapause. TGF-{beta} signaling was thought to only be required post-implantation, but we show that the ligand Nodal and its downstream effector Smad2 are essential for the survival of paused embryonic stem cells (ESCs) and blastocysts. Mechanistically, we found that Smad2 represses peroxisome-proliferator activated receptor gamma (Pparg), a transcription factor that is a master regulator of lipid storage, a process incompatible with pausing. Ablation of Pparg in Smad2-deficient ESCs rescues their survival and prevents excess lipid buildup in paused conditions. Our findings establish Nodal/Smad2 signaling as pivotal for sustaining the transcriptional and metabolic programs of embryonic diapause. This crosstalk between TGF-{beta} signaling and the Pparg pathway may be redeployed in other contexts, such as in cancer dormancy and metabolic disorders.

developmental biology↗