Introductory figure. A.

<p>Diagram of the HET-s and HET-S domain organization with a N-terminal HeLo domain and a C-terminal PFD comprising two pseudo-repeats (r1 and r2). <b>B.</b> Structure of the HET-s PFD (pdb: 2RNM), only the two pseudo-repeats and the connecting loop are shown. <b>C.</b> Mechanism of HET-S/[Het-s] incompatibility, when the HET-S PFD region interacts with the prion form of HET-s, transconformation of the C-terminal region induces refolding and activation of the HeLo toxicity domain. <b>D.</b> The “secteur” phenotype caused by the σ infectious element in <i>Nectria haematococca.</i> The arrow points to a mycelia sector in which the σ infectious element is present and leads to an alteration of the growth margin and to the secretion of a red pigment. The diagram on the right is the working model proposed by Daboussi and co-workers to account for the role of the sesA and sesB proteins. The model proposes that sesA and sesB can exist in a normal and modified form (italicized) and that the modification of sesA is autocatalytic and can also induce modification of sesB. Modified sesA leads to the red pigmentation phenotype, modification of sesB to the growth alteration characteristic of the “secteur” (redrawn after Graziani et al. 2004). <b>D.</b> Domain organization of the members of NWD-gene family of <i>P. anserina</i>. All family members share a central NACHT nucleotide binding oligomerisation domain and a C-terminal WD repeat domain but differ by their N-terminal effector domains. This effector domain is a HET cell death inducing domain (PF06985) in NWD1 to NWD5 (see text for description of the other effector domains). NWD2 lacks a N-terminal effector domain.