Regional Centre of Central Tuber Crops Research Institute, Bhubaneswar, Orissa, India Changes in Phenolics, Polyphenol Oxidase and its Isoenzyme Patterns in Relation to Resistance in Taro against Phytophthora colocasiae Manas anas Ranjan anjan Sahoo ahoo 1 , Paresh aresh Chandra handra Kole ole 2 , Madhumita adhumita Dasgupta asgupta 3 and and Archana rchana Mukherjee ukherjee 4 AuthorsÕ addresses: 1 Farm Science Centre, Orissa University of Agriculture and Technology, KVK Balasore, Baliapal, Orissa, India; 2 Department of Crop Improvement, Horticulture and Agricultural Botany, Institute of Agriculture, Visva Bharati, Sriniketan, West Bengal, India; 3 Centre for Cellular and Molecular Biology, Hyderabad, Andhra Pradesh, India; 4 Regional Centre of Central Tuber Crops Research Institute, Bhubaneswar, Orissa, India (correspondence to Manas Ranjan Sahoo. E-mail: mrsahoo2004@rediffmail.com) Received November 16, 2007; accepted April 29, 2008 Keywords: disease resistance, isoenzymes, phenolics, Phytophthora blight, polyphenol oxidase, taro Abstract The effect of Phytophthora leaf blight disease, caused by Phytophthora colocasiae Raciborski, on the accu- mulation of phenolics and polyphenol oxidase (PPO) activity in ex vitro plants was studied in three resistant (DP-25, Duradim and Jhankri) and one susceptible (N-118) genotypes of taro [Colocasia esculenta (L). Schott]. The inoculation of taro leaves with P. coloca- siae spores resulted in a quantitative change in both biochemical parameters and induction of PPO iso- forms in resistant genotypes. The amount of phenolics was increased owing to blight by 68.02%, 58.87%, 52.67% and 11.50% in DP-25, Duradim, Jhankri and N-118, respectively. The per cent increase in PPO under stress over non-stress condition was also highest in DP-25 (49.14%) followed by Duradim (41.56%), Jhankri (40.55%) and N-118 (17.08%). The resistant genotypes showed higher activity of PPO as compared with susceptible ones, which was reflected through its banding pattern in isoenzyme analysis, detecting four different isoforms. The intensity of the bands was higher in the resistant genotypes than in susceptible N-118. The appearance of high intensity bands and or reduction in the intensity of particular isoform(s) in the zymograms of all the three resistant taro genotypes studied, led to the apparent conclusion of linking PPO isoenzyme expression with blight resistance in taro. The blight incidence (per cent leaf infection and leaf area infection) was lower in the resistant genotypes than in susceptible, N-118. The yield reduction owing to blight was below 20% in DP-25, Jhankri and Dura- dim, while the same was more than 40% in N-118. The phenolics and PPO activity was negatively corre- lated with disease incidence and yield reduction owing to blight. Based on the results of disease incidence, biochemical contents and yield, the pattern of stress tolerance was DP-25 > Duradim > Jhankri > N-118. The studied parameters, i.e. phenolics and PPO could be used as biochemical markers for leaf blight stress tolerance studies in taro. Introduction Plants have several lines of defence against invading pathogens including preformed barriers and induced responses. Plant–pathogen interactions cause a com- plex network of molecular and cytological events, which provide the host susceptibility or resistance. Resistance is conferred in plants that possess several pre-existing barriers and chemical weapons in addition to pathogen-induced physical and chemical defence strategies (Hammond-Kosack and Parker, 2003). Among these defence responses are hypersensitive programmed cell death (Greenberg, 1997), induction of a large number of defence-related genes (Dixon and Harrison, 1990), biosynthesis of phytoalexins and metabolism of phenolic compounds (Hahlbrock and Scheel, 1989; Nicholson and Hammerschmidt, 1992) and production of reactive oxygen species (ROS), such as singlet oxygen, superoxide, hydrogen peroxide and hydroxyl radical (Lamb and Dixon, 1997; Mittler, 2002). A hypersensitive response at the site of infection is often manifested as necrotic lesions resulting from host cell death (Dempsey et al., 1999), and production of molecular signals that trigger systemic responses that prevent subsequent pathogen attacks not only against the attacking pathogen, but also against other types of pathogen species (Ryals et al., 1994). This defensive response, designated as systemic acquired resistance (SAR), plays an important role in disease resistance and operates through the activation of mul- tiple defence compounds at sites, distant from the point of pathogen attack (Dean and Kuc, 1985). J. Phytopathol 157:145–153 (2009) doi: 10.1111/j.1439-0434.2008.01458.x Ó 2008 The Authors Journal compilation Ó 2008 Blackwell Verlag, Berlin