Bottom-gate-type thin film transistors using ZnO as an active channel layer (ZnO–TFT) have been constructed. The ZnO layers were deposited using pulsed laser deposition at 450 °C at an oxygen pressure of 3 m Torr, and the material that was formed had a background carrier concentration of less than 5×1016 cm−3. A double layer gate insulator consisting of SiO2 and SiNx was effective in suppressing leakage current and enabling the ZnO–TFT to operate successfully. The Ion/Ioff ratio of ZnO–TFTs fabricated on Si wafers was more than 105 and the optical transmittance of ZnO–TFTs fabricated on glass was more than 80%. These results show that it is possible to fabricate a transparent TFT that can even be operated in the presence of visible light.

A similar gene network was found to control chick myogenesis, in which Six1, Eya2 and Dach2 synergistically regulate the expression of myogenic genes such as myogenin and MyoD (Heanue et Six1 is a member of the Six family homeobox genes, which function as components of the Pax-Six-Eya-Dach gene network to control organ development. Six1 is expressed in otic vesicles, nasal epithelia, branchial arches/pouches, nephrogenic cords, somites and a limited set of ganglia. In this study, we established Six1-deficient mice and found that development of the inner ear, nose, thymus, kidney and skeletal muscle was severely affected. Six1-deficient embryos were devoid of inner ear structures, including cochlea and vestibule, while their endolymphatic sac was enlarged. The inner ear anomaly began at around E10.5 and Six1 was expressed in the ventral region of the otic vesicle in the wild-type embryos at this stage. In the otic vesicle of Six1-deficient embryos, expressions of Otx1, Otx2, Lfng and Fgf3, which were expressed ventrally in the wildtype otic vesicles, were abolished, while the expression domains of Dlx5, Hmx3, Dach1 and Dach2, which were expressed dorsally in the wild-type otic vesicles, expanded ventrally. Our results indicate that Six1 functions as a key regulator of otic vesicle patterning at early embryogenesis and controls the expression domains of downstream otic genes responsible for respective inner ear structures. In addition, cell proliferation was reduced and apoptotic cell death was enhanced in the ventral region of the otic vesicle, suggesting the involvement of Six1 in cell proliferation and survival. In spite of the similarity of otic phenotypes of Six1-and Shh-deficient mice, expressions of Six1 and Shh were mutually independent.

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Six4 is a member of the Six family genes, homologues of Drosophila melanogaster sine oculis. The gene is thought to be involved in neurogenesis, myogenesis, and development of other organs, based on its specific expression in certain neuronal cells of the developing embryo and in adult skeletal muscles. To elucidate the biological roles of Six4, we generated Six4-deficient mice by replacing the Six homologous region and homeobox by the ␤-galactosidase gene. 5-Bromo-4-chloro-3-indolyl-␤-D-galactopyranoside staining of the heterozygous mutant embryos revealed expression of Six4 in cranial and dorsal root ganglia, somites, otic and nasal placodes, branchial arches, Rathke's pouch, apical ectodermal ridges of limb buds, and mesonephros. The expression pattern was similar to that of Six1 except at the early stage of embryonic day 8.5. Six4-deficient mice were born according to the Mendelian rule with normal gross appearance and were fertile. No hearing defects were detected. Six4-deficient embryos showed no morphological abnormalities, and the expression patterns of several molecular markers, e.g., myogenin and NeuroD3 (neurogenin1), were normal. Our results indicate that Six4 is not essential for mouse embryogenesis and suggest that other members of the Six family seem to compensate for the loss of Six4.

The transposition frequency of Tam3 in Antirrhinum majus, unlike that of most other cut-and-paste-type transposons, is tightly controlled by temperature: Tam3 transposes rarely at 25°C, but much more frequently at 15°C. Here, we studied the mechanism of the low-temperature-dependent transposition (LTDT) of Tam3. Our results strongly suggest that LTDT is not likely to be due to either transcriptional regulation or posttranscriptional regulation of the Tam3 TPase gene. We found that temperature shift induced a remarkable change of the methylation state unique to Tam3 sequences in the genome: Higher temperature resulted in hypermethylation, whereas lower temperature resulted in reduced methylation. The methylation state was reversible within a single generation in response to a temperature shift. Although our data demonstrate a close link between LTDT and the methylation of Tam3, they also suggest that secondary factor(s) other than DNA methylation is involved in repression of Tam3 transposition.Tam3 in Antirrhinum majus is exceptional among cut-and-paste-type transposons (TEs) in that it is the only known TE whose transpositional behavior can be strictly controlled by environmental influence. Tam3 transposition is strongly affected by temperature: It is active at low temperatures (around 15°C) and stable at high temperatures (around 25°C; Harrison and Fincham, 1964). Shifting the temperature controls the activity mitotically and probably meiotically. Based on a study of variegation spots, Carpenter et al. (1987) reported that the Tam3 excision rate was approximately 1,000-fold greater at 15°C than at 25°C. Thus, Tam3 is remarkably sensitive to the growth temperature. This trait has provided a great advantage for the isolation and analysis of a variety of genes involved in pigmentation and development in A. majus (Coen et al., 1989).Among the regulatory factors associated with TE activity, DNA methylation is widely involved in the inhibition of transpositional events in plant TEs. DNA methylation can regulate TE transposition at the levels of both transposase (TPase) gene expression and the TPase binding process (Schlappi et al., 1994;Ros and Kunze, 2001). Martin et al. (1989) suggested that Tam3 inactivation is also associated with DNA methylation. Kitamura et al. (2001) showed that at high temperatures, the repression of transposition occurs simultaneously for all Tam3 copies in the genome, whereas at low temperatures, the repression is released to various degrees depending on the location of the copies. The degree of the Tam3 transposition activity was found to be influenced by chromosomal position and related to the degree of methylation of the element ends.Here, we attempted to find differences between the active and inactive states of Tam3 in plants grown at different temperatures. We compared the amounts of the transcript of the TPase gene and compared the enzymatic activity of Tam3 TPase between plants grown at 25°C and 15°C. The results showed that neither the transcription of the TPase gene nor its enzy...