Viroid Pathogenicity One Process, Many Faces 英文参考文献.docVIP

Viruses 2009, 1, 298-316; doi:10.3390/v1020298 OPEN ACCESS viruses ISSN 1999-4915 /journal/viruses Review Viroid Pathogenicity: One Process, Many Faces Robert A. Owens * and Rosemarie W. Hammond Molecular Plant Pathology Laboratory, USDA/ARS, Beltsville, MD 20705, USA; E-mail: rose.hammond@ * Author to whom correspondence should be addressed; E-mail: robert.a.owens@; Tel.: +1-301-504-6209; Fax: +1-301-504-5449. Received: 14 July 2009; in revised form: 31 August 2009 / Accepted: 1 September 2009 / Published: 10 September 2009 Abstract: Despite the non-coding nature of their small RNA genomes, the visible symptoms of viroid infection resemble those associated with many plant virus diseases. Recent evidence indicates that viroid-derived small RNAs acting through host RNA silencing pathways play a key role in viroid pathogenicity. Host responses to viroid infection are complex, involving signaling cascades containing host-encoded protein kinases and crosstalk between hormonal and defense-signaling pathways. Studies of viroid-host interaction in the context of entire biochemical or developmental pathways are just beginning, and many working hypotheses have yet to be critically tested. Keywords: viroid pathogenicity; RNA silencing; disease induction Introduction Even before the non-coding nature of viroid genomes had been established, how such a small RNA molecule could induce disease was a matter of intense interest. In a 1971 paper comparing the properties of potato spindle tuber “virus” with those of conventional plant viruses and proposing the existence of a new class of pathogens to be known as viroids, T.O. Diener suggested that the genome of Potato spindle tuber viroid (PSTVd) might function, not as a messenger RNA, but rather as an abnormal regulatory RNA [1]. Several years later, determination of its complete nucleotide sequence confirmed the non-cod