Mouse genetics identifies unique and overlapping functions of fibroblast growth factor receptors in keratinocytes

Fibroblast growth factors (FGFs) are key regulators of tissue development, homeostasis and repair, and abnormal FGF signalling is associated with various human diseases. In human and murine epidermis, FGF receptor 3 (FGFR3) activation causes benign skin tumours, but the consequences of FGFR3 deficiency in this tissue have not been determined. Here, we show that FGFR3 in keratinocytes is dispensable for mouse skin development, homeostasis and wound repair. However, the defect in the epidermal barrier and the resulting inflammatory skin disease that develops in mice lacking FGFR1 and FGFR2 in keratinocytes were further aggravated upon additional loss of FGFR3. This caused fibroblast activation and fibrosis in the FGFR1/FGFR2 double-knockout mice and even more in mice lacking all three FGFRs, revealing functional redundancy of FGFR3 with FGFR1 and FGFR2 for maintaining the epidermal barrier. Taken together, our study demonstrates that FGFR1, FGFR2 and FGFR3 act together to maintain epidermal integrity and cutaneous homeostasis, with FGFR2 being the dominant receptor

Expression of Xyloglucanase (AaXEG2) in Open-field-grown Poplars

The transgenic expression of Aspergillus aculeatus xyloglucanase with 35S promoter, which has been maintained in greenhouse-grown transgenic poplars for 10 years, was assessed to determine their expression level in open-field-grown poplars. This level was slightly decreased in the poplars grown in fertile soil for four years, and there were proportionatel y decreased levels of xyloglucanase activity among their tissues, in which the shoots exhibited slightly lower specific activities than was observed in the leaves and roots. Xyloglucan content was greatly decreased in the walls of the tissues in the transgenic lines, although the degradation levels of xyloglucan were slightly lower for the poplars grown in fertile soil than for those grown in non-fertile soil. The results showed that the level of expression, together with xyloglucan degradation in their walls, was decreased for the poplars grown in fertile soil

Monazite geochronology and geochemistry of meta-sediments in the Narryer Gneiss Complex, Western Australia: Constraints on the tectonothermal history and provenance

Mt. Narryer and Jack Hills meta-sedimentary rocks in the Narryer Gneiss Complex of the Yilgarn Craton, Western Australia are of particular importance because they yield Hadean detrital zircons. To better understand the tectonothermal history and provenance of these ancient sediments, we have integrated backscattered scanning electron images, in situ U-Pb isotopic and geochemical data for monazites from the meta-sediments. The data indicate multiple periods of metamorphic monazite growth in the Mt. Narryer meta-sediments during tectonothermal events, including metamorphism at ~3.3-3.2 and 2.7-2.6 Ga. These results set a new minimum age of 3.2 Ga for deposition of the Mt. Narryer sediments, previously constrained between 3.28 and ~2.7 Ga. Despite the significant metamorphic monazite growth, a relatively high proportion of detrital monazite survives in a Fe- and Mn-rich sample. This is likely because the high Fe and Mn bulk composition resulted in the efficient shielding of early formed monazite by garnet. In the Jack Hills meta-sediments, metamorphic monazite growth was minor, suggesting the absence of high-grade metamorphism in the sequence. The detrital monazites provide evidence for the derivation of Mt. Narryer sediments from ca. 3.6 and 3.3 Ga granites, likely corresponding to Meeberrie and Dugel granitic gneisses in the Narryer Gneiss Complex. No monazites older than 3.65 Ga have been identified, implying either that the source rocks of >3.65 Ga detrital zircons in the sediments contained little monazite, or that >3.65 Ga detrital minerals had experienced significant metamorphic events or prolonged sedimentary recycling, resulting in the complete dissolution or recrystallization of monazite. © 2010 Springer-Verlag