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Tetsuji Nagatani,Maromu Yamada,Tomoko Kojima,Daizhou Zhang 한국대기환경학회 2012 Asian Journal of Atmospheric Environment (AJAE) Vol.6 No.1
Particulate sulfate in PM2.5, sulfur dioxide (SO2) and size-segregated aerosol particle number concentrations were measured at a site (32° 9′N, 129° 59′E) on the southwestern Japan coast from 5 March to 10April, 2010. Results show frequent episodic increases of sulfate and SO2. Compared to the average concentration of sulfate 4.4±2.7 μg m-3 in the whole observation period, episodic sulfate reached 10.5-20.1 μg m-3. The variation of sulfate always synchronized with aerosol particles in the size range of 0.1-0.5 μm,indicating the episodic sulfate was a consequence of the increase of the sub-micron particles. SO2 did not have remarkable increase in any episodes of sulfate increase. During the passage of low pressure systems which loaded Asian dust in postfrontal air, concentrated sulfate appeared right behind the front but before dust arrival, suggesting the dominance of dustfree particulate sulfate. Weather and backward trajectory analyses revealed that air parcels with high sulfate passed eastern and northeastern China or Korean peninsula before arriving at the site. In contrast,those with high SO2 passed an active volcano,Mt. Sakurajima, about 100 km in the south, suggesting the SO2 was more likely from the volcanic emission. The ratio of sulfate to total sulfur compounds (SO42-)/(SO42-+SO2) was 0.31-0.89 in continentally originated air while was 0.25-0.43 in the air having passed the volcano, showing more efficient conversions of SO2 to sulfate in the air from the continent. The close dependence of the conversion on humidity in the continentally originated air was confirmed. Particulate sulfate in PM2.5, sulfur dioxide (SO2) and size-segregated aerosol particle number concentrations were measured at a site (32° 9′N, 129° 59′E) on the southwestern Japan coast from 5 March to 10April, 2010. Results show frequent episodic increases of sulfate and SO2. Compared to the average concentration of sulfate 4.4±2.7 μg m-3 in the whole observation period, episodic sulfate reached 10.5-20.1 μg m-3. The variation of sulfate always synchronized with aerosol particles in the size range of 0.1-0.5 μm,indicating the episodic sulfate was a consequence of the increase of the sub-micron particles. SO2 did not have remarkable increase in any episodes of sulfate increase. During the passage of low pressure systems which loaded Asian dust in postfrontal air, concentrated sulfate appeared right behind the front but before dust arrival, suggesting the dominance of dustfree particulate sulfate. Weather and backward trajectory analyses revealed that air parcels with high sulfate passed eastern and northeastern China or Korean peninsula before arriving at the site. In contrast,those with high SO2 passed an active volcano,Mt. Sakurajima, about 100 km in the south, suggesting the SO2 was more likely from the volcanic emission. The ratio of sulfate to total sulfur compounds (SO42-)/(SO42-+SO2) was 0.31-0.89 in continentally originated air while was 0.25-0.43 in the air having passed the volcano, showing more efficient conversions of SO2 to sulfate in the air from the continent. The close dependence of the conversion on humidity in the continentally originated air was confirmed.
Phytochrome B inhibits binding of phytochrome‐interacting factors to their target promoters
Park, Eunae,Park, Jeongmoo,Kim, Junghyun,Nagatani, Akira,Lagarias, J. Clark,Choi, Giltsu Blackwell Publishing Ltd 2012 The Plant journal Vol.72 No.4
<P><B>Summary</B></P><P>Phytochromes are red and far‐red light receptors in plants that mediate critical responses to light throughout the lifecycle. They achieve this in part by targeting negatively acting bHLH transcription factors called phytochrome‐interacting factors (PIFs) for degradation within the nucleus. However, it is not known whether protein degradation is the primary mechanism by which phytochromes inhibit these repressors of photomorphogenesis. Here, we use chromatin immunoprecipitation to show that phyB inhibits the regulatory activity of PIF1 and PIF3 by releasing them from their DNA targets. The N‐terminal fragment of phyB (NG‐GUS‐NLS; NGB) also inhibits binding of PIF3 to its target promoters. However, unlike full‐length phyB, NGB does not promote PIF3 degradation, establishing the activity of NGB reflects its ability to inhibit PIF binding to DNA. We further show that Pfr forms of both full‐length phyB and NGB inhibit DNA binding of PIF1 and PIF3 <I>in vitro</I>. Taken together, our results indicate that phyB inhibition of PIF function involves two separate processes: sequestration and protein degradation.</P>