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Neurogenesis is the generation of neurons from stem cells, a process that is regulated by SoxB transcription factors (TFs) in many animals. Although the roles of these TFs are well understood in bilaterians, how their neural function evolved is unclear. Here, we use Hydractinia symbiolongicarpus , a member of the early-branching phylum Cnidaria, to provide insight into this question. Using a combination of mRNA in situ hybridization, transgenesis, gene knockdown, transcriptomics, and in vivo imaging, we provide a comprehensive molecular and cellular analysis of neurogenesis during embryogenesis, homeostasis, and regeneration in this animal. We show that SoxB genes act sequentially at least in some cases. Stem cells expressing Piwi1 and Soxb1 , which have broad developmental potential, become neural progenitors that express Soxb2 before differentiating into mature neural cells. Knockdown of SoxB genes resulted in complex defects in embryonic neurogenesis. Hydractinia neural cells differentiate while migrating from the aboral to the oral end of the animal, but it is unclear whether migration per se or exposure to different microenvironments is the main driver of their fate determination. Our data constitute a rich resource for studies aiming at addressing this question, which is at the heart of understanding the origin and development of animal nervous systems. 

In bilaterians and cnidarians, epithelial cell-polarity is regulated by the interactions between Par proteins, Wnt/PCP signaling pathway, and cell-cell adhesion. Par proteins are highly conserved across Metazoa, including ctenophores. But strikingly, ctenophore genomes lack components of the Wnt/PCP pathway and cell-cell adhesion complexes raising the question if ctenophore cells are polarized by mechanisms involving Par proteins. Here, by using immunohistochemistry and live-cell imaging of specific mRNAs, we describe for the first time the subcellular localization of selected Par proteins in blastomeres and epithelial cells during the embryogenesis of the ctenophore Mnemiopsis leidyi . We show that these proteins distribute differently compared to what has been described for other animals, even though they segregate in a host-specific fashion when expressed in cnidarian embryos. This differential localization might be related to the emergence of different junctional complexes during metazoan evolution. 

Most animals – including birds, fish and mammals – have symmetrical left and right sides, and are known as bilaterians. During early life, the embryos of animals in this group develop three distinct layers of cells: the ectoderm (outer layer), the endoderm (inner layer), and the mesoderm (middle layer). These layers then go on to form the animal’s tissues and organs. The ectoderm produces external tissues, such as the skin and the nervous system; the endoderm forms internal tissues, like the gut; and the mesoderm creates all tissues in between, like muscles and blood. Another, smaller group of animals, called cnidarians, do not have left and right sides. Instead, they have a ‘radial symmetry’, meaning they have multiple identical parts arranged in a circle. These animals – which include corals, jellyfish and sea anemones – only develop two distinct layers of cells, equivalent to the outer and inner layers of bilaterians. Cnidarians evolved before bilaterians, but their genetic material is equally complex. So why did these two groups evolve to have different layers of cells? And how exactly do animal embryos develop these distinct layers? To address these questions, Salinas-Saavedra et al. studied embryos of the sea anemone Nematostella vectensis. Molecules called Par-proteins play an important role in controlling how cells behave and attach to one another (and therefore how they form layers). So, using a technique called immunohistochemistry to look inside cells, Salinas-Saavedra et al. examined these proteins in the two layers of cells in sea anemone embryos. The experiments found that in the sea anemones, Par-proteins are arranged differently in cells that form the ‘skin’ compared to cells that form the ‘gut’. In other words, cells in the outer layer attach to one another in a different way than cells in the inner layer, where the Par-proteins are degraded by ‘mesodermal’ genes. The findings also show that these sea anemones have all they need to form a third middle layer of cells. Like bilaterians, they could potentially move cells in and out of sheets that line surfaces inside the body – but they do not naturally do this. Understanding how animals form different layers of cells is important for scientists studying evolution and the development of embryos. However, it also has wider applications. For instance, some cells involved in developing the mesoderm are also involved in forming tumors. Future research in this area could help scientists learn more about how cancer-like cells form in animals. 

Abstract N6‐methyldeoxyadenosine (6mA) is a chemical alteration of DNA, observed across all realms of life. Although the functions of 6mA are well understood in bacteria and protists, its roles in animal genomes have been controversial. We show that 6mA randomly accumulates in early embryos of the cnidarianHydractinia symbiolongicarpus, with a peak at the 16‐cell stage followed by clearance to background levels two cell cycles later, at the 64‐cell stage—the embryonic stage at which zygotic genome activation occurs in this animal. Knocking downAlkbh1, a putative initiator of animal 6mA clearance, resulted in higher levels of 6mA at the 64‐cell stage and a delay in the initiation of zygotic transcription. Our data are consistent with 6mA originating from recycled nucleotides of degraded m6A‐marked maternal RNA postfertilization. Therefore, while 6mA does not function as an epigenetic mark inHydractinia, its random incorporation into the early embryonic genome inhibits transcription. In turn, Alkbh1 functions as a genomic 6mA “cleaner,” facilitating timely zygotic genome activation. Given the random nature of genomic 6mA accumulation and its ability to interfere with gene expression, defects in 6mA clearance may represent a hitherto unknown cause of various pathologies.