Fate-mapping experiments in the mouse have revealed that the primitive streak can be divided into three functional regions: the proximal region gives rise to germ cells and the extra-embryonic mesoderm of the yolk sac; the distal region generates cardiac mesoderm and node-derived axial mesendoderm; and the middle streak region produces the paraxial, intermediate and lateral plate mesoderm of the trunk. To gain insight into the mechanisms that mediate the assembly of the primitive streak into these functional regions, we have cloned and functionally identified the gene disrupted in the amnionless (amn) mouse, which has a recessive, embryonic lethal mutation that interferes specifically with the formation and/or specification of the middle primitive streak region during gastrulation. Here we report that the gene Amn encodes a novel type I transmembrane protein that is expressed exclusively in the extra-embryonic visceral endoderm layer during gastrulation. The extracellular region of the Amn protein contains a cysteine-rich domain with similarity to bone morphogenetic protein (BMP)-binding cysteine-rich domains in chordin, its Drosophila melanogaster homolog (Short gastrulation) and procollagen IIA (ref. 3). Our findings indicate that Amn may direct the production of trunk mesoderm derived from the middle streak by acting in the underlying visceral endoderm to modulate a BMP signaling pathway.
Reduction of wild-type activity of the polychaetoid (pyd) gene results in formation of extra mechanosensory bristles on the head and notum of adult Drosophila. Loss of pyd function results in decreased ability to restrict sensory organ precursor (SOP) formation to a single cell per proneural cluster. Although the initial proneural cluster pattern of achaete expression is not altered in pyd mutants, extra cells within proneural clusters express the high levels of achaete characteristic of SOPs. This observation suggests that pyd+ functions as a negative regulator of achaete-scute complex expression within the proneural cluster. Synergistic interactions between pyd and Notch, Delta and extramacrochaetae mutations support this model. We also demonstrate that pyd is required for normal eye development.
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