This study investigates the effects of PDGF B deficiency in mice, which are essential for growth, migration, and function of mesenchymal cells. Mice deficient in PDGF B die perinatally and exhibit several anatomical and histological abnormalities. Key findings include: 1. **Renal Abnormalities**: Kidney glomeruli fail to form due to the absence of mesangial cells. Instead, a single or a few distended capillary loops fill the glomerular space, leading to a "spotty kidney phenotype." 2. **Cardiovascular Abnormalities**: The heart and large arteries dilate in late-stage embryos. Enlarged and deformed hearts, dilated thoracic aorta, and hypertrabeculated ventricular walls are observed. 3. **Hematological Abnormalities**: Most PDGF B mutant embryos develop fatal hemorrhages just before birth. They exhibit erythroblastosis, macrocytic anemia, and thrombocytopenia. 4. **Phenotypic Analysis**: PDGF B mutants show increased nucleated erythrocytes and reduced platelet counts. Hematological changes become more pronounced at E19, correlating with the extent of bleeding. 5. **Mechanisms**: The failure of mesangial cell development in the kidneys may be due to impaired migration, proliferation, or function. The arterial dilation suggests a failure of smooth muscle cell function, possibly related to vasoconstriction. 6. **Implications**: The phenotype of PDGF B-negative mouse embryos reflects functions specific to PDGF B-containing dimers (PDGF BB and PDGFB) and/or overlapping functions with other proteins. The development of the glomerular mesangium likely involves PDGF BB signaling through PDGFRβ dimers. 7. **Conclusion**: PDGF B plays crucial roles in establishing certain renal and circulatory functions, highlighting its importance in vivo.This study investigates the effects of PDGF B deficiency in mice, which are essential for growth, migration, and function of mesenchymal cells. Mice deficient in PDGF B die perinatally and exhibit several anatomical and histological abnormalities. Key findings include: 1. **Renal Abnormalities**: Kidney glomeruli fail to form due to the absence of mesangial cells. Instead, a single or a few distended capillary loops fill the glomerular space, leading to a "spotty kidney phenotype." 2. **Cardiovascular Abnormalities**: The heart and large arteries dilate in late-stage embryos. Enlarged and deformed hearts, dilated thoracic aorta, and hypertrabeculated ventricular walls are observed. 3. **Hematological Abnormalities**: Most PDGF B mutant embryos develop fatal hemorrhages just before birth. They exhibit erythroblastosis, macrocytic anemia, and thrombocytopenia. 4. **Phenotypic Analysis**: PDGF B mutants show increased nucleated erythrocytes and reduced platelet counts. Hematological changes become more pronounced at E19, correlating with the extent of bleeding. 5. **Mechanisms**: The failure of mesangial cell development in the kidneys may be due to impaired migration, proliferation, or function. The arterial dilation suggests a failure of smooth muscle cell function, possibly related to vasoconstriction. 6. **Implications**: The phenotype of PDGF B-negative mouse embryos reflects functions specific to PDGF B-containing dimers (PDGF BB and PDGFB) and/or overlapping functions with other proteins. The development of the glomerular mesangium likely involves PDGF BB signaling through PDGFRβ dimers. 7. **Conclusion**: PDGF B plays crucial roles in establishing certain renal and circulatory functions, highlighting its importance in vivo.