bioRxiv Science⌕ Search

bioRxiv · 10.1101/2022.12.15.519123

Cell-specific occupancy dynamics between the pioneer-like factor Opa/ZIC and Ocelliles/OTX regulate early head development in embryos

Abstract

During development, embryonic patterning systems direct a set of initially uncommitted pluripotent cells to differentiate into a variety of cell types and tissues. A core network of transcription factors, such as Zelda/POU5F1, Odd-paired (Opa)/ZIC and Ocelliless (Oc)/OTX, are conserved across animals. While Opa is essential for a second wave of zygotic activation after Zelda, it is unclear whether Opa drives head cell specification past gastrulation onset, in the Drosophila embryo. Our hypothesis is that Opa and Oc are interacting with distinct cis-regulatory regions for shaping cell fates in the embryonic head. Using super-resolution microscopy and epigenomic meta-analysis of single cell RNAseq datasets we find that opas and ocs overlapping expression domains are dynamic in the head region, with both factors being simultaneously transcribed at the blastula stage. However, analysis of single-embryo RNAseq data reveals a subgroup of Opa-bound genes to be Opa-independent in the cellularized embryo. Interrogation of these genes against Oc ChIPseq combined with in situ data, suggests that Opa is competing with Oc for the regulation of a subgroup of genes later in gastrulation. Specifically, we find that Oc binds to late, head-specific enhancers independently and activates them in a head-specific wave of zygotic transcription, suggesting distinct roles for Oc in the blastula and gastrula stages.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Fenelon, K., Gao, F., Borad, P., Abbasi, S., Pachter, L., Koromila, T.. 2022-12-16. Cell-specific occupancy dynamics between the pioneer-like factor Opa/ZIC and Ocelliles/OTX regulate early head development in embryos. https://doi.org/10.1101/2022.12.15.519123

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

KEEP EXPLORING

Related preprints

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↗

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↗

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↗