Factors regulating the formation of the intermediate mesoderm are not fully understood. It is believed that bone morphogenic proteins, or BMPs, specify regions of growth along the dorsal-ventral axis of the mesoderm and plays a central role in formation of the intermediate mesoderm. Vg1/ signalling is an identified regulator of intermediate mesoderm formation acting through BMP signalling. Excess Vg1/Nodal signalling during early gastrulation stages results in expansion of the intermediate mesoderm at the expense of the adjacent paraxial mesoderm, whereas inhibition of Vg1/Nodal signalling represses intermediate mesoderm formation. A link has been established between Vg1/Nodal signalling and BMP signalling, whereby Vg1/Nodal signalling regulates intermediate mesoderm formation by modulating the growth-inducing effects of BMP signalling. Other necessary markers of intermediate mesoderm induction include the odd-skipped related gene and paired-box-2 gene which require intermediate levels of BMP signalling to activate Markers of early intermediate mesoderm formation are often not exclusive to the intermediate mesoderm. This can be seen in early stages of intermediate mesoderm differentiation where higher levels of BMP stimulate growth of lateral plate tissue, whilst lower concentrations lead to paraxial mesoderm and somite formation. Osr1, which encodes a zinc-fingerDNA-binding protein, and LIM-type homeobox gene expression overlaps the intermediate mesoderm as well as the lateral plate. Osr1 has expression domains encompassing the entire length of the anterior-posterior axis from the first somites. It is not until the 4th-8th somite stage that markers with greater specificity to the intermediate mesoderm are identified including Pax2/8 genes activated from the 6th somite. Lhx1 expression also becomes more restricted to the intermediate mesoderm. Genetic analyses in animal studies show that Lhx1, Osr1 and Pax2/8 signalling are all critical in specification of the intermediate mesoderm into its early derivatives.
Derived Organs and Tissues
As development proceeds, the intermediate mesoderm differentiates sequentially along the anterior-posterior axis into three successive stages of the early mammalian and avian urogenital system, named pronephros, mesonephros and metanephros respectively. The intermediate mesoderm will eventually develop into the kidney and parts of both male and female reproductive systems.
Kidneys
Early kidney structures include the pronephros and mesonephros, whose complexity, size and duration can vary greatly between vertebrate species. The adult kidney, also referred to as the metanephric kidney, forms at the posterior end of the intermediate mesoderm after the degeneration of previous, less complex kidney structures.
Pronephros
During early development, the pronephric duct forms from the intermediate mesoderm, ventral to the anterior somites. The cells of the pronephric duct migrate caudally whilst inducing adjacent mesenchyme to form the tubules of the initial kidney-like structure called the pronephros. This process is regulated by Pax2/8 markers. The pronephros is active in adult forms of some primitive fish and acts as the primary excretory system in amphibious larvae and embryonic forms of more advanced fish. In mammals however, the pronephric tubules and the anterior portion of the pronephric duct degenerates in 3.5 weeks to be succeeded by the mesonephros, the embryonic kidney.
Mesonephros
The mesonephros is constituted of a set of new tubules formed from the lateral and ventral sides of the gonadal ridge joining the cloaca. The mesonephros functions between the 6th and 10th weeks of embryological life of mammals as a temporary kidney, but serves as the permanent excretory organ of aquatic vertebrates. By 8 weeks post-conception, the human mesonephros reaches maximum size and begins to regress, with complete regression occurring by week 16. Despite its transiency, the mesonephros is crucial for the development of structures such as the Wolffian duct, which in turn gives rise to the ureteric bud of the metanephric kidney.
, also known as nephroblastoma, is an embryonic tumor originating from metanephric blastemal cells that are incapable of completing the mesenchymal-epithelial transition, a crucial process during kidney differentiation involving the transition from a multipolar, spindle-shaped mesenchymal cell to a planar assembly of polarized epithelial cells. As a consequence, WTs have a triphasic histology composed of three morphogenically distinct cell types: undifferentiated blastemal cells, epithelial cells, and stromal cells. The Wnt/βcatenin signalling pathway is crucial for initiating MET, where specifically the WNT4 protein is required for induction of epithelial renal vesicles and the transition from mesenchymal to epithelial cells. WTs are often a result of a genetic deletions or inactivating mutations in WT1, which subsequently inhibits Wnt/βcatenin signalling and prevents MET progression.