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Disease cycle of potato late blight - MSpace at the University of ...

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infestans secretes both cytoplasmic and apoplastic effectors (Kamoun 2005). For<br />

example, serine protease inhibitors EPI1 and EPI10 are apoplastic effectors th<strong>at</strong> are<br />

thought to function in <strong>the</strong> counter-defense inhibiting PR protein P69B, a subtilisin-like<br />

serine protease <strong>of</strong> tom<strong>at</strong>o (Tian et al. 2005). In <strong>pot<strong>at</strong>o</strong>, Wang et al. (2004b) reported th<strong>at</strong><br />

an aggressive P. infestans US8 strain suppresses host defense mechanisms through<br />

transcriptional inhibition <strong>of</strong> phenylpropanoid (PAL) and isoprenoid (HMGR) p<strong>at</strong>hways<br />

(Wang et al. 2008).<br />

Up-regul<strong>at</strong>ion <strong>of</strong> defense-re<strong>l<strong>at</strong>e</strong>d genes such as those controlling chitinase, beta-<br />

glucanase, and o<strong>the</strong>r p<strong>at</strong>hogenesis-re<strong>l<strong>at</strong>e</strong>d proteins in both comp<strong>at</strong>ible and incomp<strong>at</strong>ible<br />

plant-p<strong>at</strong>hogen interactions is well documented (Maleck et al. 2000). However, genes<br />

expressed in an incomp<strong>at</strong>ible interaction and represented in a cDNA library do not all<br />

correspond to critical inform<strong>at</strong>ion for future studies on resistance genes, especially when<br />

<strong>the</strong> same gene is also expressed in <strong>the</strong> comp<strong>at</strong>ible interaction counterpart.<br />

Cases where up-regul<strong>at</strong>ion occurs only in <strong>the</strong> susceptible or <strong>the</strong> resistant line, and<br />

only in response to ei<strong>the</strong>r <strong>the</strong> virulent or avirulent strain <strong>of</strong> <strong>the</strong> p<strong>at</strong>hogen, have rarely been<br />

described (Valer et al. 2006). Also, during both incomp<strong>at</strong>ible and comp<strong>at</strong>ible interactions,<br />

many p<strong>at</strong>hogens are invasive and establish p<strong>at</strong>hogenic structures within <strong>the</strong> host tissue.<br />

As a result, it is difficult to separ<strong>at</strong>e <strong>the</strong> p<strong>at</strong>hogen tissue from th<strong>at</strong> <strong>of</strong> <strong>the</strong> host, and both<br />

are represented in <strong>the</strong> pool <strong>of</strong> expressed genes from <strong>the</strong> interaction.<br />

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