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Fruit melanotic ringspot (FMRS) – a disease of resistant Capsicum genotypes infected with Tomato spotted wilt virus (TSWV) on the fruits

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Etiology of pepper fruit melanotic ringspot (FMRS) disease (Salamon, 2009) was studied on fruit samples collected in forced pepper populations. It was noticed that in spite of heavy thrips (Frankliniella occidentalis) infestations and of TSWV epidemy detected in the forcing houses, FMRS occurred only in plants having healthy foliage. Symptomatological surveys strongly suggested that FMRS appeared exclusively in specific pepper genotypes. The size of melanotic ringspots has been observed to grow at room temperature during postripening of diseased fruits. A mechanically transmitted plant virus was isolated from symptomatic parts of 9 white pepper fruits affected by FMRS. On test plants each of the virus isolates caused systemic symptoms characteristic to TSWV. Using cDNA/PCR technique and TSWV N-gene specific primers a ca. 300 bp long DNA fragment has been amplified from total nucleic acid extracted from symptomatic tissues but never from asymptomatic parts of the fruits showing FMRS. Plant progenies grown from seeds of FMRS diseased fruits segregated in respect of resistance and/or susceptibility to TSWV infection. TSWV was also detected in and isolated from three fruits showed non-melanotic yellow rings (one of them was infected with a tobamovirus, too). Seedlings derived from these fruits proved to be susceptible to TSWV. Based on the above results we could conclude that the FMRS disease developed on fruits of “cecei” type white peppers that carry a TSWV resistance gene, most likely the Tsw gene in heterozygous form. These fruits were infected with thrips transmitted TSWV and FRMS appeared as a hypersentive reaction (HR) manifested in fruits.
Title: Fruit melanotic ringspot (FMRS) – a disease of resistant Capsicum genotypes infected with Tomato spotted wilt virus (TSWV) on the fruits
Description:
Etiology of pepper fruit melanotic ringspot (FMRS) disease (Salamon, 2009) was studied on fruit samples collected in forced pepper populations.
It was noticed that in spite of heavy thrips (Frankliniella occidentalis) infestations and of TSWV epidemy detected in the forcing houses, FMRS occurred only in plants having healthy foliage.
Symptomatological surveys strongly suggested that FMRS appeared exclusively in specific pepper genotypes.
The size of melanotic ringspots has been observed to grow at room temperature during postripening of diseased fruits.
A mechanically transmitted plant virus was isolated from symptomatic parts of 9 white pepper fruits affected by FMRS.
On test plants each of the virus isolates caused systemic symptoms characteristic to TSWV.
Using cDNA/PCR technique and TSWV N-gene specific primers a ca.
300 bp long DNA fragment has been amplified from total nucleic acid extracted from symptomatic tissues but never from asymptomatic parts of the fruits showing FMRS.
Plant progenies grown from seeds of FMRS diseased fruits segregated in respect of resistance and/or susceptibility to TSWV infection.
TSWV was also detected in and isolated from three fruits showed non-melanotic yellow rings (one of them was infected with a tobamovirus, too).
Seedlings derived from these fruits proved to be susceptible to TSWV.
Based on the above results we could conclude that the FMRS disease developed on fruits of “cecei” type white peppers that carry a TSWV resistance gene, most likely the Tsw gene in heterozygous form.
These fruits were infected with thrips transmitted TSWV and FRMS appeared as a hypersentive reaction (HR) manifested in fruits.

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