Letter to the Editor Reply to commentary by A. Fisette on the article “Relationship between the acylation-stimulating protein gene and coronary heart disease in the Xinjiang Uygur and Han populations of China” published in Genetics and Molecular Research 13 (2):

Abstract

In answer to the questioning of the terminology we used in our manuscript (Chen et al., 2014), ASP is a 76-amino acid (8932 Da) fragment, which is identical to C3adesArg, a cleavage product of complement C3. Cleavage of complement C3 is mediated via the alternate complement pathway by the interaction of C3, factor B and adipsin (Factor D, a serine protease enzyme), which generates C3a. Rapid cleavage of the C terminal arginine of C3a by carboxypeptidase N generates ASP (Hugli, 1990). Activation of this pathway is initiated through the C3b component of C3 (ASP precursor) associated with the plasma membrane. In the presence of Mg 2+ , Factor B binds to the activated C3b to form a C3bB complex. This, in turn, induces a conformational change of Factor B, permitting proteolytic cleavage by adipsin. The action of adipsin on C3b-bound Factor B generates a C3bBb fragment (a C3 convertase),

Drought stress-induced changes of microRNAs in diploid and autotetraploid Paulownia tomentosa

“…Pau-miR159, which was up-regulated in PT2 vs. PT2T and did not change in PT4 vs. PT4T, was predicted to target GAMYB . This gene family is the largest transcription factor family in plants, and is a component of gibberellin signaling, The differential expression of GAMYB was reported to influence the promoter activity of the most predominant gibberellin-responsive gene RAmy1A in the gibberellin signaling pathway (Washio and Washio 2014). These results suggest that drought stress responses are very complicated is controlled by a various signaling net,and the co-ordination of pau-miR4–target and pau-miR159–target regulation might promote drought tolerance in P. tomentosa .…”