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Investigating the mechanisms that restrict the extra-embryonic Yolk Syncytial Layer

Investigating the mechanisms that restrict the extra-embryonic Yolk Syncytial Layer
研究限制胚胎外卵黄合胞层的机制
批准号:
BB/X001539/1
负责人:
Karuna Sampath
金额:
$53.03万
依托单位:
依托单位国家:
英国
项目类别:
Research Grant
财政年份:
2022
资助国家:
英国
项目状态:
未结题
起止时间:
2022 至 --

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中文摘要
翻译
许多动物的正常发育取决于构成动物的细胞(“胚胎细胞”)以及本身不形成最终动物形式的一部分的支持细胞(“胚外”细胞)。例如,人类胎盘是一种支持性的“胚胎外”组织,对正常的人类胚胎发育至关重要。在许多鱼类物种中,称为卵黄合胞体层(YSL)的胚外组织在共享的卵黄细胞质中发育。YSL不会成为完全形成的动物的一部分,但对于发育中的鱼类来说,它是营养和信号的重要来源。如果发育中的鱼胚胎在非常早期的阶段与蛋黄和YSL分离,则胚胎发育异常。虽然YSL对正常发育至关重要,但它是如何形成的以及如何控制YSL还没有很好的了解。由母亲沉积到卵子中的蛋白质因子被认为控制YSL的形成,但迄今为止,只发现了少数分子,并且它们在YSL发育中的作用还不清楚。我们发现,缺乏蛋白质Igf2bp3和Ybx1的斑马鱼胚胎以胚胎本身为代价,具有异常扩大的YSL,导致胚胎的灾难性后果。Igf2bp3和Ybx1如何控制YSL的形成尚不清楚。斑马鱼胚胎在早期阶段是透明的,因此可以在YSL形成时看到它。我们将拍摄正常斑马鱼胚胎中形成的YSL,并与缺乏这些蛋白质的胚胎进行比较。我们将研究在YSL形成过程中这些蛋白质是如何控制一些关键的细胞通讯途径的。我们将确定Igf2bp3和Ybx1控制YSL发展的关键分子。通过这些策略,我们将发现Igf2bp3和Ybx1在斑马鱼YSL形成中的功能。这两种蛋白质都存在于许多动物中。我们确定的机制可能涉及其他鱼类的胚外组织形成。因此,这项工作可能与动物物种的胚胎外发育具有广泛的相关性。
英文摘要
The normal development of many animals depends on cells that make the animal ("embryonic cells") as well as supporting cells that do not form a part of the final animal form per se ("extra-embryonic" cells). For instance, the human placenta is a supporting "extra-embryonic" tissue which is essential for normal human embryo development. In many fish species, an extra-embryonic tissue called the yolk syncytial layer (YSL) develops within a shared yolk cytoplasm. The YSL does not become a part of the fully-formed animal, but is a crucial source of nutrition and signals for the developing fish. If the developing fish embryo is separated from the yolk and YSL at very early stages, the embryo develops abnormally. Although the YSL is crucial for normal development, how it forms and how the YSL is controlled is not well understood. Protein factors deposited by the mother into the egg are thought to control YSL formation, but to date, only a few molecules have been found and how they act in YSL development is not well understood. We found that Zebrafish embryos lacking the proteins Igf2bp3 and Ybx1 have an abnormally expanded YSL at the expense of the embryo proper, leading to disastrous consequences for the embryo. How Igf2bp3 and Ybx1 control YSL formation is not known. Zebrafish embryos are transparent at early stages, making it possible to see the YSL as it forms. We will film the YSL as it forms in normal zebrafish embryos and compare to embryos lacking these proteins. We will investigate how some key cell communication pathways are controlled by these proteins during YSL formation. We will identify the key molecules through which Igf2bp3 and Ybx1 control development of the YSL. Through these strategies, we will find out how Igf2bp3 and Ybx1 function in YSL formation in zebrafish. Both the proteins are present in many animals. The mechanisms that we identify might be involved in extra-embryonic tissue formation in other fish. Therefore, the work is likely to be of broad relevance to extra-embryonic development across animal species.
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