Notes on Ceratocystis paradoxa causing internal post-harvest rot disease on immature coconut in Brazil

Abstract

Currently there is a large and increasing demand for immature coconuts for fresh consumption of their liquid endosperm (coconut water). The occurrence of post-harvest diseases prevent its sale and change the taste, making it inappropriate for consumption. In 2011, coconut fruits showing internal post-harvest rot symptoms were found in a market in Belo Horizonte and after incubation for 5 days in a humid chamber at room temperature, fungal structures were observed. Fruiting structures show morphology typical of Ceratocystis paradoxa. For molecular identification, DNA sequences were generated for the Internal Transcribed Spacer regions 1 and 2 including the 5.8S rRNA gene, part of the β-tubulin and the Transcription Elongation Factor 1-α gene regions. These data were compared with those of other C. paradoxa using phylogenetic analysis. Koch's postulates was confirmed by inoculation of 6-mm-diameter PDA plugs with the isolate on fruits of coconut. Morphology of the isolates in culture as well as phylogenetic inference showed that the causal agent of internal post-harvest rot disease on coconut is C. paradoxa.

Diagrammatic scale of severity for postharvest black rot (Ceratocystis paradoxa) in coconut palm fruits

“…Considering coconut fruit production, which is destined to fresh fruit commercialization and exportation for coconut water consumption, that fungal species was recently identified causing fruit rot or fruit black rot (15). Diseases caused by this fungus, leading to postharvest losses, have also affected other fruit crops such as peach palm (10), cocoa (14), date palm (19), pineapple (3) and banana (2).…”

“…Etiology and epidemiology of this disease have not been studied accordingly to define economically reasonable control strategies. Symptoms in the fruits could vary according to the phenological stage, the environmental conditions and the diversity of the pathogen population since virulence in fruits is little known (15) Ceratocystis paradoxa incidence and damage to the Brazilian coconut crop have been apparently neglected until recently. Although it has often been the first cause of the disease in this country (25,26), Alves & Lourd (1) reported this fungus causing immature fruit drop and affecting coconut production.…”

“…The two diseases are similar in early stages of symptom development in harvested fruits, making difficult to reach the correct diagnosis which, in this case, could be obtained based on indirect isolation or presence of signs of the pathogen. Black rot intensity varies according to the environmental conditions and the presence of a latent fungus; internal rot can also be observed, even in green coconuts, making their commercialization unfeasible and changing the taste of their water (22,15).…”

Phylogeography and population structure analysis reveals diversity by mutations in Lasiodiplodia theobromae with distinct sources of selection

“…Mycelium pure cultures were macerated inside tubes containing pellets of 1.4 mm in diameter and 600 µL Nuclei Lysis Solution; then, the tubes were placed into a cell disruptor (Loccus L-Beader 3) three times at 3700 rpm for 40 s; the other DNA extraction steps were done as reported by Pinho et al (2013).…”

Postharvest rot and mummification of strawberry fruits caused by Neofusicoccum parvum and N. kwambonambiense in Brazil

“…The target sequences of the ITS region, 28S rDNA, β-tubulin, TEF1-α and RPB2 were amplified using the primers ITS1 (5'-TCC GTA GGT GAA CCT GCG G-3') and ITS4 (5'-TCC TCC GCT TAT TGA TAT GC-3') for ITS (White et al, 1990), LR0R (5'-ACC CGC TGA ACT TAA GC-3') and LR5 (5'-TCC TGA GGG AAA CTT CG-3') for the partial 28S rDNA (Vilgalys & Hester, 1990), T1 (5'-AAC ATG CGT GAG ATT GTA AGT-3') and Bt2b (5'-ACC CTC AGT GTA GTG ACC CTT GGC-3') for the partial β-tubulin (Glass & Donaldson, 1995;O'Donnell & Cigelnik, 1997), EF1F (5'-TGC GGT GGT ATC GAC AAG CGT-3') and EF2R (5'-AGC ATG TTG TCG CCG TTG AAG-3') for the partial TEF1-α (Jacobs et al, 2004) and 5F2 (5'-GGG GWG AYC AGA AGA AGG C-3)' and 7cR (5'-CCC ATR GCT TGY TTR CCC AT-3') for the partial RPB2 (Sung et al, 2007;Liu et al, 1999) following the protocols of Pinho et al (2013) and Sung et al (2007). Amplification of ITS, β-tubulin, TEF1-α and RPB2 produced sequences of approximately 550, 630, 680 and 860 bp, respectively.…”