Molecular characterisation of Cyclaneusma spp. from New Zealand plantations
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Formerly known as the Forest Research Institute, Scion has been a leader in research relating to forest health for over 50 years. The Rotorua-based Crown Research Institute continues to provide science that will protect all forests from damage caused by insect pests, pathogens and weeds. The information presented below arises from these research activities.
From Forest Health News 245, February 2014.
Cyclaneusma needle-cast (CNC) is a foliar disease of Pinus radiata that has been known to cause a major impact on growth in some regions of New Zealand. The disease is caused by Cyclaneusma minus of which there are at least two morphological types in New Zealand. Recent molecular research by Australian colleagues has confirmed that these two morphotypes, termed “simile” and “verum”1, could in fact be separate species (Prihatini et al. manuscript in preparation).
In New Zealand, we do not know the role of the two different morphotypes in causing CNC. Previous research looking at the distribution of the two morphotypes showed that “simile” was more common in the North Island and less common in the South Island. However, populations varied between forests, and also varied at locations between collection periods.
Over the past summer Shannon Hunter, an Auckland University student, has been working on molecular characterization of the Cyclaneusma spp. from the Scion Reference Laboratory Culture Collection. The isolates had been made from collections taken from 1969 to 2011 and in total 76 isolates were analysed. The results of these analyses showed that the most prevalent morphotype was Cyclaneusma minus “simile” and this morphotype is found throughout New Zealand. DNA sequence analysis of additional genetic regions showed separate phylogenetic grouping of the two morphotypes as observed in the study by Prihatini et al. providing further support for the morphotypes being separate species.
This preliminary study will support future research analysing the genetic diversity of the morphotypes to form a better understanding of their roles in either promoting or inhibiting CNC disease.
Rebecca McDougal & Shannon Hunter
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