Fuelling phytoremediation: gasoline degradation by green wall systems-a case study.

The capacity for indoor plants including green wall systems to remove specific volatile organic compounds (VOCs) is well documented in the literature; however under realistic settings, indoor occupants are exposed to a complex mixture of harmful compounds sourced from various emission sources. Gasoline vapour is one of the key sources of these emissions, with several studies demonstrating that indoor occupants in areas surrounding gasoline stations or with residentially attached garages are exposed to far higher concentrations of harmful VOCs. Here we assess the potential of a commercial small passive green wall system, commercially named the 'LivePicture Go' from Ambius P/L, Australia, to drawdown VOCs that comprise gasoline vapour, including total VOC (TVOC) removal and specific removal of individual speciated VOCs over time. An 8-h TVOC removal efficiency of 42.45% was achieved, along with the complete removal of eicosane, 1,2,3-trimethyl-benzene, and hexadecane. Further, the green wall also effectively reduced concentrations of a range of harmful benzene derivatives and other VOCs. These results demonstrate the potential of botanical systems to simultaneously remove a wide variety of VOCs, although future research is needed to improve upon and ensure efficiency of these systems over time and within practical applications.

The role of formins in human disease.

Formins are a conserved family of proteins that play key roles in cytoskeletal remodeling. They nucleate and processively elongate non-branched actin filaments and also modulate microtubule dynamics. Despite their significant contributions to cell biology and development, few studies have directly implicated formins in disease pathogenesis. This review highlights the roles of formins in cell division, migration, immunity, and microvesicle formation in the context of human disease. In addition, we discuss the importance of controlling formin activity and protein expression to maintain cell homeostasis.

Distinct but overlapping functions for the closely related p190 RhoGAPs in neural development.

The p190 RhoGAPs, p190A and p190B, are highly related GTPase-activating proteins for the Rho GTPases. Rho GTPases and p190A reportedly control various aspects of brain development, and we hypothesized that p190B would be likewise involved in neuronal development. We find that like p190A, p190B is prominently expressed in the developing and adult brain. Unlike p190A, p190B is not abundantly tyrosine phosphorylated. We further demonstrate, using p190B-deficient mice, that p190B is required for normal brain development. Mice lacking p190B display several major defects, including (1) deficits in the formation of major forebrain commissures, including the corpus callosum and anterior commissure, (2) dilation of the lateral ventricles, suggesting inhibition of neurogenesis and/or survival, (3) thinning of the neocortical intermediate zone, suggesting defects in neuronal differentiation and/or axonal outgrowth, and (4) impaired neuronal differentiation. These defects are similar to, but distinct from, those described in p190A-deficient mice. RNA interference-mediated knockdown of neither p190 protein results in significant inhibition of neurite outgrowth in neuroblastoma cells, despite an apparent increase in RhoA activity. We conclude that p190 RhoGAPs control pivotal aspects of neural development, including neuronal differentiation and process outgrowth, and that these effects are mediated by signaling systems that include, but are not limited to, RhoA.

Modulation of CREB activity by the Rho GTPase regulates cell and organism size during mouse embryonic development.

Rho GTPases regulate several aspects of tissue morphogenesis during animal development. We found that mice lacking the Rho-inhibitory protein, p190-B RhoGAP, are 30% reduced in size and exhibit developmental defects strikingly similar to those seen in mice lacking the CREB transcription factor. In p190-B RhoGAP-deficient mice, CREB phosphorylation is substantially reduced in embryonic tissues. Embryo-derived cells contain abnormally high levels of active Rho protein, are reduced in size, and exhibit defects in CREB activation upon exposure to insulin or IGF-1. The cell size defect is rescued by expression of constitutively activated CREB, and in wild-type cells, expression of activated Rho or dominant-negative CREB results in reduced cell size. Together, these results suggest that activity of the Rho GTPase modulates a signal from insulin/IGFs to CREB that determines cell size and animal size during embryogenesis.