Quercus suber infected by Phytophthora cinnamomi: effects at cellular level of cinnamomin on roots, stem and leaves

Phytophthora cinnamomi has been reported to be regularly associated with cork and holm oak decline. This oomycete secretes elicitins, a group of unique highly conserved pr oteins that can enhance plant defence reactions

Loss of Aggressiveness of Phytophthora cinnamomi (Beta-Cinnamomin Silenced Strain) in the Infection of Castanea sativa

Several forest species are severely affected by Phytophthora cinnamomi. The contribution of this oomycete to forest decline and dieback has been broadly reported. In particular, it is consensual that it is the causal agent of ink disease in Castanea sativa. It has been associated with the severe decline of Quercus species, namely the Q. suber and Q. ilex dieback in Portugal and Spain, and has been responsible for the infection of numerous native species and crops. This pathogen persists in the soil or on plant material in the form of chlamydospores allowing the infection of living root tissues when environmental conditions are favorable. © Microscopy Society of America 2012

Involvement of the beta-cinnamomin elicitin in infection and colonisation of cork oak roots by Phytophthora cinnamomi

The virulence of two wild type (PA45 and PA37) and two genetically modified (13C: hygromycin resistant; FATSS: hygromycin resistant and β-cin knock-down) Phytophthora cinnamomi strains towards cork oak (Quercus suber) was assessed via a quantitative evaluation of disease symptoms arising from a soil infestation assay, and by a istological analysis of root colonization. Comparison of virulence, as expressed by symptom severity, resulted in the following ranking: highly virulent (wild type strains), medium virulence (strain 13C) and weakly virulent (FATSS). Both transgenic strains were compromised in their virulence, as expressed by symptom severity, but strain 13C was much less affected than FATSS. Microscopic observation showed that the FATSS strain was unable to effectively invade the root, while 13C and the two wild type strains were all able to rapidly colonize the whole root, including the vascular tissue. These results strengthen the notion that elicitins are associated, either directly or indirectly, with the infection process of Phytophthora

Studies on the association of the Quercus suber decline disease with Phytophthora cinnamomi in Portugal

In Portugal, the decline disease has been described in evergreen oaks (Quercus suber L. and Q.ilex subsp. rotundifolia Lam.) since the end of the 19th century. The mortality of these species affects, particularly the central and southern regions of the country, being one of the most severe forest problems. Phytophthora cinnamomi Rands is the main pathogen responsible for the cork and holm oak mortality in Portugal. Several studies have been developed aiming at a better understanding of the effect of the P. cinnamomi action on the cork oak trees decline. The present work describes preliminary results of some of these studies

Exposition of cork oak roots to cryptogein reduced the Infection by Phytophtora cinnamomi

The oomycete P. cinnamomi has been described as strong contributing factor to the decline of cork oak and holm oak stands occurring in the Iberian Peninsula. There are no eradication methods available against this pathogen

Alpha cinnamomin elicits a defence response against Phytophthora cinnamomi in Castanea sativa

Phytophthora cinnamomi and P. cambivora are considered as the causal agents of Castanea sativa ink disease. These soil-borne plant pathogens invade and destroy the root system leading to the death of the trees. Most Phytophthora species secrete elicitins, a group of unique highly conserved proteins that are able to enhance plant defence responses in a systemic acquired resistance manner against infection by several pathogens. A cluster of four elicitin genes was identified in P. cinnamomi. In previous works one of these elicitins, α- cinnamomin was shown to restrict the invasion of root cortical tissues by P. cinnamomi preventing vascular colonization in cork and holm oak. In the present work, roots of chestnut plantlets grown in vitro were allowed to absorb α-cinnamomin at 100 μg/ml for two days before being inoculated with P. cinnamomi. The effects of this elicitin on host-pathogen interaction were studied at histological and ultrastructural levels. P. cinnamomi was restricted to the outer cortex of 65% of the roots pre-treated with α-cinnamomin. In these roots, the vascular cylinders were free of pathogen. On the contrary, the pathogen reached the vascular cylinder, penetrating the phloem and xylem vessels in all non-treated assayed roots. The signs of pathogen degradation in the cortical parenchyma, mainly in the intercellular spaces, and the increase of a physical barrier in epidermal and sub-epidermal cell wall-media lamella and intercellular spaces by impregnation with phenol-like compounds strongly suggest that α-cinnamomin induced in chestnut defence reactions against P. cinnamomi

A utilização de elicitinas no combate contra Phytophthora cinnamomi na doença da tinta do castanheiro e no declínio do montado

Phytophthora cinnamomi e P. cambivora são considerados os agentes patogénicos da doença da tinta do castanheiro. Estes agentes invadem e destroem o sistema radicular, levando à morte das árvores e a importantes perdas económicas. O declínio do montado tem sido associado a vários agentes patogénicos, pragas e factores abióticos. Phytophthora cinnamomi tem sido referido como um potencial agente patogénico do sobreiro e azinheira. O aparecimento de mais estirpes de microrganismos patogénicos resistentes a pesticidas impõe o desenvolvimento de novas estratégias de biocontrolo, entre as quais a estimulação de reações de defesa. As elicitinas são proteínas de baixo peso molecular, secretadas por algumas espécies de oomycetes (Phytophthora e Pythium) que induzem reações de hipersensibilidade e aquisição de resistência sistémica nas plantas, contra um grande número de bactérias e fungos patogénicos. Este trabalho é uma síntese dos resultados sobre o efeito da aplicação radicular de várias elicitinas, na infeção do sobreiro, azinheira e castanheiro por P. cinnamomi. A avaliação foi efetuada por observação microscópica dos tecidos invadidos, em especial dos tecidos vasculares. Observou‑se a indução de reações de defesa contra P. cinnamomi quando se submeteram as raízes destas três espécies a pré‑tratamento com as elicitinas criptogeína, capsiceína ou cinamomina. A infeção ficou restrita aos tecidos corticais da raiz, onde o agente patogénico se desorganizou e não progrediu para os vasos, estando associado à acumulação de materiais que se presume serem tóxicos, produzidos nas células dos hospedeiros, em contato com as hifas em desorganização. Os ensaios laboratoriais indicaram que as elicitinas testadas se revelaram muito eficientes no biocontrolo de P. cinnamomi. Será de grande importância desenvolver tecnologia no sentido de obtenção de elicitinas a baixo custo e de criar sistemas eficientes da sua dispersão nas plantas

Germline MUTYH (MYH) mutations in Portuguese individuals with multiple colorectal adenomas

Germinal mutations in the base excision repair (BER) gene MUTYH (MYH) have recently been described in association with predisposition to multiple colorectal adenomas and cancer. In contrast to the classic dominant condition of familial adenomatous polyposis (FAP) due to germinal mutations in the APC gene, the MYH polyposis is an autosomal recessive disease. The identification of individuals affected by MYH polyposis brings new and important implications for the diagnostic, screening, genetic counseling, follow up and therapeutic options in these patients. In this study, screening for germinal mutations in the MYH gene was performed in 53 Portuguese individuals with multiple colorectal adenomas or classic adenomatous polyposis, in whom no mutation had been identified in the APC gene. The results revealed the presence of biallelic germline MYH mutations in 21 patients. In addition, we here report 3 mutations (c.340T>C [p.Y114H]; c.503G>A [p.R168H]; and c.1186_1187insGG [p.E396fsX437]) which, to our knowledge, have not been previously describe