Smad4 controls proliferation of interstitial cells in the neonatal kidney.

Expansion of interstitial cells in the adult kidney is a hallmark of chronic disease, whereas their proliferation during fetal development is necessary for organ formation. An intriguing difference between adult and neonatal kidneys is that the neonatal kidney has the capacity to control interstitial cell proliferation when the target number has been reached. In this study, we define the consequences of inactivating the TGFß/Smad response in the mouse interstitial cell lineage. We find that pathway inactivation through loss of Smad4 leads to overproliferation of interstitial cells regionally in the kidney medulla. Analysis of markers for BMP and TGFß pathway activation reveals that loss of Smad4 primarily reduces TGFß signaling in the interstitium. Whereas TGFß signaling is reduced in these cells, marker analysis shows that Wnt/ß-catenin signaling is increased. Our analysis supports a model in which Wnt/ß-catenin-mediated proliferation is attenuated by TGFß/Smad to ensure that proliferation ceases when the target number of interstitial cells has been reached in the neonatal medulla.

Developmental and adult expression of semaphorin 2a in the cricket Gryllus bimaculatus.

Developmental guidance cues act to direct growth cones to their correct targets in the nervous system. Recent experiments also demonstrate that developmental cues are expressed in the adult mammalian nervous system, although their function in the brain is not yet clear. The semaphorin gene family has been implicated in the growth of dendrites and axons in a number of different species. While the expression of semaphorin and its influence on tibial pioneer neurons in the developing limb bud have been well characterized in the grasshopper, the expression of semaphorin 2a (sema2a) has not been explored in the adult insect. In this study we used polymerase chain reaction (PCR) with degenerate and gene-specific primers to clone part of the secreted form of sema2a from Gryllus bimaculatus. Using in situ hybridization and immunohistochemistry, we confirmed that sema2a mRNA and protein expression patterns in the embryonic cricket were similar to that seen in the grasshopper. We also showed that tibial neuron development in crickets was comparable to that described in grasshopper. An examination of both developing and adult cricket brains showed that sema2a mRNA and protein were expressed in the Kenyon cells in mushroom bodies, an area involved in learning and memory. Sema2a expression was most obvious near the apex of the mushroom body in a region surrounding the neurogenic tip, which produces neurons throughout the life of the cricket. We discuss the role of neurogenesis in learning and memory and the potential involvement of semaphorin in this process.

White mutants of Chlamydomonas reinhardtii are defective in phytoene synthase.

Carotenoids play an integral and essential role in photosynthesis and photoprotection in plants and algae. A collection of Chlamydomonas reinhardtii mutants lacking carotenoids was characterized for pigment and tocopherol (vitamin E) composition, growth phenotypes under different light conditions, and the molecular basis of their mutant phenotype. The carotenoid-less mutants, or "white" mutants, were also deficient in chlorophylls but had approximately twice the tocopherol content of the wild type. White mutants grew in the dark but were unable to survive in the light, even under very low light conditions on acetate-containing medium. Genetic crosses and recombination tests revealed that all individual white mutants in the collection are alleles of a single gene, lts1, and the white phenotype was closely linked to a marker located in the phytoene synthase gene. DNA sequencing of the phytoene synthase gene from each of the mutants revealed nonsense, missense, frameshift, and splice site mutations. Transformation with a wild-type copy of the phytoene synthase gene was able to complement the lts1-210 mutation. Together, these results show that all the white mutants examined in this work are affected in the phytoene synthase gene.