bioRxiv Science⌕ Search
Home/Archive/bioRxiv

bioRxiv · 10.1101/2023.12.03.569790

Spontaneous Intersibling Polymorphism in the Development of Dopaminergic Neuroendocrine Cells in Sea Urchin Larvae: Impacts on the Expansion of Marine Benthic Species

Obukhova, A. L.·Khabarova, M. Y.·Semenova, M. N.·Starunov, V. V.·Voronezhskaya, E. E.·Ivashkin, E. G.
View original source ↗Export metadata ↓

Abstract

Plasticity of the nervous system enables the formation of the most adaptive neural circuits and the corresponding behavior of animals. The mechanism by which plasticity arises during development and its involvement in animal adaptation is one of the astonishing questions. Sea urchin larvae are known for their evolutionary and ecological diversity as well as their developmental forms and behavioral patterns. This research addresses the intricate neuroendocrine adaptations that govern larval development of sea urchins, focusing on the coordination between dopaminergic (DA) and serotonergic (5-HT) neurons. The study reveals a heterochronic polymorphism in the appearance of post oral DA neurons and confirms the stable differentiation pattern of apical 5-HT neurons in the larvae of Mesocentrotus nudus and Paracentrotus lividus. We demonstrate that an increased number of DA cells and DA application correlate with downward swimming of the larvae. In contrast, 5-HT cells and serotonin application unsure larval upward swimming. As a result, the 5-HT/DA ratio underlay stage-dependent vertical distribution of the larvae within the water column. In larvae of the same age, the precise balance of 5-HT and DA cells underlie the basis for the different potentials of individuals for upward and downward swimming. This coordination in humoral regulation underlies shifts in larval behavior within a single generation. Based on our findings on DA-cells polymorphism, we have proposed a model illustrating how the balance between the serotonin and dopamine systems, shaped by heterochrony in DA cell appearance, impacts larval behavior, reduces competition between siblings and ensures optimal population expansion. The study explores the evolutionary and ecological implications of these neuroendocrine adaptations in marine species.

Source connections

Explore related subjects

developmental biologyPreprint

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Obukhova, A. L., Khabarova, M. Y., Semenova, M. N., Starunov, V. V., Voronezhskaya, E. E., Ivashkin, E. G.. 2023-12-05. Spontaneous Intersibling Polymorphism in the Development of Dopaminergic Neuroendocrine Cells in Sea Urchin Larvae: Impacts on the Expansion of Marine Benthic Species. https://doi.org/10.1101/2023.12.03.569790

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

bioRxiv2026

Neural regulation of hatching in amphibians

Many animal embryos hatch in response to threats or opportunities, yet how cue sensing activates hatching is unknown. We screened red-eyed treefrog (Agalychnis callidryas) eggs in the field with small molecules to discover that the neurotransmitter acetylcholine is a key mediator of hatching enzyme release. Using behavioral pharmacology, microscopy, and transcriptional profiling we identify direct cholinergic input on hatching gland cells that triggers enzyme release for egg rupture, and serotonergic transduction of embryonic hypoxia sensing. Independent hypoxia-sensing and mechanosensory predation-detection pathways converge on a hatching decision that elicits acetylcholine-dependent enzyme release and coordinated hatching-specific behavior. Cholinergic regulation of hatching enzyme release is conserved in a distantly related frog and salamander, suggesting a shared ancestral hatching mechanism. These results provide a neural basis for hatching plasticity which may have contributed to the evolution of diverse hatching modes in amphibians.

developmental biology↗
bioRxiv2026

Towards Understanding the Microenvironmental Control of Reindeer Antler Regeneration

Deer antlers are the only mammalian appendages capable of complete periodic regeneration and therefore provide a natural model for investigating mechanisms of skeletal regeneration. However, current knowledge of the structural and molecular characteristics of the regenerative antler microenvironment remains incomplete. Here, we compared antler tip and antler base tissues from Rangifer tarandus (reindeer) with mature metacarpal cortical bone using structural, compositional, histological, and proteomic analyses. Antler tissues exhibited smaller and less crystalline apatite structures, elevated carbonate substitution, and higher organic matrix content compared with metacarpal bone, indicating an immature mineral phase. Antlers also exhibited lower bone mineral density, greater porosity, reduced bone volume fraction, and greater trabecular separation, particularly in central regions, consistent with a dynamic remodeling microenvironment. Histological examination revealed abundant active osteons and extensive osteoid seams in antler tissues, whereas metacarpal bone predominantly comprised mature lamellar bone with limited remodeling activity. Proteomic profiling identified distinct extracellular matrix signatures between antler and metacarpal tissues. Metacarpal bone was enriched in proteins associated with skeletal homeostasis, mechanotransduction, and bone remodeling, whereas antler tissues were enriched in proteins involved in extracellular matrix reorganization, metabolic adaptation, and regeneration. Collectively, these findings indicate that reindeer antlers possess a specialized regenerative skeletal microenvironment characterized by immature mineral organization, active remodeling, and distinct molecular signatures associated with rapid tissue growth. These results provide new insights into the biological basis of mammalian appendage regeneration and may facilitate the development of regenerative strategies for bone repair and skeletal tissue engineering.

developmental biology↗
bioRxiv2026

Endogenous expression of mutant RagC in mice results in early-onset dilated cardiomyopathy with features of the Long-Olsen-Distelmaier syndrome

Dilated cardiomyopathy (DCM) is a severe heart condition often linked to arrhythmias, clots, and heart failure, for which treatments are not yet curative. Recently, de novo mutations in genes encoding components of the Rag GTPase nutrient signaling pathway, particularly in RRAGC, have been found in unrelated patients with a severe, early-onset DCM syndrome called Long-Olsen-Distelmaier. Cancer cell lines, hiPSC-derived cardiomyocytes and zebrafish have been used to study this Ragopathy, but a mammalian model to investigate this syndrome has not been generated. Here, we show that mice engineered to endogenously express mutations in Serine 74 (orthologous to the Serine 75 mutated in patients), exhibit early-onset features of DCM with decreased heart size, fibrosis, diastolic dysfunction and aortic insufficiency, characteristics reminiscent of the human syndrome. Moreover, Rragc-mutant hearts display decreased left ventricular mass and interventricular septum. Endogenous heterozygous expression of Rragc mutant variants result in a milder, sublethal defective physiological cardiac growth with increased systolic and diastolic blood pressure. Mechanistically, active RagC does not cause abnormal increase in cardiomyocyte size, but leads to suppressed transcriptional activity of Tfeb and alterations in cardiomyocyte metabolism. Transcriptional profiling of neonatal mutant hearts reveals multiple signatures of impaired mitochondrial activity. Ex vivo and in vitro analyses of murine cardiomyocyte mitochondria from Rragc-mutant mice show suppressed mitochondrial respiration, disturbed complex IV multimerization and super-complex organization. These data point to abnormal early postnatal heart metabolism by deregulated nutrient - Rag GTPase signaling with a potential molecular explanation to the early onset of DCM in patients with de novo missense mutations in RRAGC, and suggests the relevance of early metabolic interventions in conditions with altered nutrient signaling

developmental biology↗