The Journal of Heredity 2002:93(1)
© 2002 The American Genetic Association 93:50-52
Brief Communication |
Inheritance of Disease Lesion Mimic Leaf Trait in Groundnut
From the Groundnut and EGFF Section, Gamma Field, Nuclear Agriculture and Biotechnology Division, Bhabha Atomic Research Centre, Trombay, Mumbai 400 085, India.
Address correspondence to G. S. S. Murty at the address above or e-mail: egffs{at}magnum.barc.ernet.in.
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Abstract |
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In groundnut, two identical mutants with disease lesion mimic leaf trait were isolated independently from two different parents through induced mutagenesis and in vitro culture technique. The leaf chlorophyll content in both the mutants was found to be drastically reduced. The segregation pattern in the F2 and F3 generations for normal and mutant traits fitted a 13:3 ratio, indicating that the disease lesion mimic trait in the mutants was due to suppressive gene action. Both mutants were allelic for the disease mimic trait.
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Introduction |
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TopAbstractIntroductionMaterials and MethodsResults and DiscussionReferences |
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In groundnut (Arachis hypogaea L.), the occurrence of several chlorophyll mutants was reported either spontaneously (Hammons 1973) or through induced mutagenesis (Patil 1966). In our groundnut breeding program, two phenotypically identical mutants were isolated and designated as TG 18AM and TAG 24M. They were derived through gamma ray treatment of seeds of TG 18A (Chandra Mouli and Kale 1982) and in vitro plant development through somatic embryogenesis from cultured immature embryonal axes (Eapen S, personal communication) of cv. TAG 24 (Patil et al. 1995). Leaves of both the mutants mimic the symptoms of groundnut rust disease (Puccinia arachidis Speg.). Several independent disease lesion mimics (DLM) have been identified in many species including groundnut (Branch 1998; Dangl et al. 1996; Greenberg and Ausubel 1993; Johal et al. 1995). Lesion mimics are normally inherited either as recessive or dominant traits (Johal et al. 1995). The objective of the present study was to investigate the inheritance and the allelic relationship of the DLM leaf trait in both the mutants in groundnut.
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Materials and Methods |
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TopAbstractIntroductionMaterials and MethodsResults and DiscussionReferences |
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Crosses were made between (1) TG 18AM and normal leaf genotypes TG 18A, TAG 24, TG 28A (A. hypogaea ssp. fastigiata) and ICGV 86564 (A. hypogaea ssp. hypogaea), (2) TAG 24M and TAG 24, and (3) TG 18AM and TAG 24M. From F1 to F3 generations, plants were advanced as plant to row progenies and segregation for normal and mutant phenotypes were scored. The distribution of DLM scores was fitted to expected ratios by using the chi-square test. The chlorophyll content in the mutants and their parents was estimated (Arnon 1949) by taking fresh leaf discs from upper and lower leaves from 65-day-old field-grown plants.
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Results and Discussion |
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TopAbstractIntroductionMaterials and MethodsResults and DiscussionReferences |
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Mutants TG 18AM and TAG 24M were characterized by erect habit, sequential flowering, and rose seed coat, resembling their parents. Hammons (1973) reported a rusty-leaf mutant, with semierect habit and pink seed coat isolated in cv. Virginia Bunch 67. In the seedling stage of both the mutants, the lower-most four to five leaves remain green. Subsequently, newly opened leaves have light green color with yellow specks, which start from the leaflet tip and progress toward the leaflet base. Coalescence of specks results in yellow blotches, which gradually spread to make the whole leaflet yellow. Simultaneously, brown specks start appearing and cover the entire leaflet, resembling rust disease symptoms in groundnut. With the advancement of age, the lower leaves gradually turn green. Thus within the same plant the unopened leaf on the main axis will have a few yellow specks and the 10th–12th leaf below the shoot apex will have green color with or without brown specks. Leaves on branches exhibit a similar pattern.
Dietrich et al. (1994) classified lesion mimics into determinate and indeterminate types. In the determinate type, lesion initiation occurs spontaneously at a particular leaf age, but lesion expansion is slow and restricted. In the indeterminate type, once lesion initiation is triggered, lesion expansion is rapid and unchecked, leading to premature leaf death. Accordingly, the present lesion mimic mutants fall into the determinate class.
Many mimics showed necrotic lesions that appeared similar to lesions characteristic of the pathogen-induced hypersensitivity reaction (Antonio et al. 1999; Dangl et al. 1996; Dietrich et al. 1994; Greenberg et al. 1994; Wolter et al. 1993). It is also unlikely that all lesion mimics are aberrations of plant responses to pathogens (Hu et al. 1998). The mimic phenotype of mutants was observed in the field both under natural rust infestation and its absence, indicating that the mutant trait is independent of the hypersensitivity reaction induced in other mimics.
The chlorophyll content in fresh leaves of mutants was drastically reduced compared to their parents (Table 1). Chlorophyll a, chlorophyll b, and total chlorophyll in the upper leaves of mutants were much lower than in the respective parents. Proportionately, chlorophyll b was much reduced compared to chlorophyll a, as revealed by higher chlorophyll a:b ratios in mutants; this was particularly more pronounced in TAG 24M. Contrary to their parents, in DLM mutants total chlorophyll increased with the age of the leaf. The upper leaves of TG 18AM and TAG 24M contained only 29% and 14% total chlorophyll of respective lower leaves.
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In the F1 and F2 generations, all plants from the cross TG 18AM x TAG 24M showed the DLM leaf trait, indicating that the genes governing this trait in both the genotypes were allelic, although they were derived from different parents and methods. All the F1 plants from seven crosses between mutants and normal leaf genotypes had green leaves. In F2 generations, segregation patterns fit well to a ratio of 13 normal:3 DLM phenotypes (Table 2). Reciprocal crosses (1) TG 18AM and TG 18A and (2) TG 18AM and ICGV 86564 did not show differences from the expected 13:3 ratio, indicating the absence of maternal or cytoplasmic effects for this trait. Pooled and homogeneity chi-square values also fit well to the 13:3 ratio (Table 2). In the F3 generation, genotypic segregation for mutant and normal phenotypes (Table 2) fit well to an expected ratio of 7 (all normal):2 (3 normal:1 mutant):4 (13 normal:3 mutant):2 (1 normal:3 mutant):1 (all mutant). Thus phenotypic and genotypic segregation in the F2 and F3 generations confirmed that the DLM leaf trait was due to suppressive gene action. A deviation from the 13:3 ratio in the F3 generation for TAG 24 x TAG 24M and TG 18AM x TAG 24 could be due to involvement of lethal factors. This was confirmed by lethality test, wherein deviation was observed for the 47 normal:5 mutant ratio from F2 normal parents and a 1 normal:5 mutant ratio from F2 mutant parents.
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Branch (1998) reported that two complementary recessive genes were responsible for the rusty-leaf trait in groundnut. Differences in the nature of gene action for this trait could be due to differences in the subspecies of these genotypes. A rusty-leaf mutant belonged to A. hypogaea ssp. hypogaea, while TG 18AM and TAG 24M belong to A. hypogaea ssp. fastigiata. Lesion mimic expression is developmentally programmed and is readily affected by the genetic background of the plant (Dangl et al. 1996; Johal et al. 1995). Impaired activity of uroporphyrinogen decarboxylase (UROD) in maize and protoporphyrinogen oxidase (PPO) in Arabidopsis, key enzymes in the biosynthetic pathway of chlorophyll and heme in plants, resulted in DLM phenotypes (Antonio et al. 1999; Hu et al. 1998). Thus an event with similar impairment might have occurred in both of our mutants, leading to the DLM leaf trait.
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Acknowledgments |
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We thank R. K. Sachan for making the crosses used in this study.
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Footnotes |
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Corresponding Editor: Prem P. Jauhar
Received March 2, 2001
Accepted November 26, 2001
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References |
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TopAbstractIntroductionMaterials and MethodsResults and DiscussionReferences |
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Antonio M, Sandy V, Dave G, Klaus M, John R, and Eric W, 1999. Inhibition of protoporphyrinogen oxidase expression in Arabidopsis causes a lesion-mimic phenotype that induces systemic acquired resistance. Plant J 17:667–678.[CrossRef][Web of Science][Medline]
Arnon DI, 1949. Copper enzymes in isolated chloroplast: phenol oxidases in Beta vulgaris. Plant Physiol 24:1–15.
Branch WD, 1998. Inheritance of a rusty-leaf trait in peanut. J Hered 89:365–366.
Chandra Mouli and Kale DM, 1982. Gamma-ray induced Spanish bunch mutant with large pod groundnut. Oleagineux 37:583–588.
Dangl JL, Dietrich RA, and Richberg MH, 1996. Death don't have no mercy: cell death programs in plant-microbe interactions. Plant Cell 8:1793–1807.[CrossRef][Web of Science][Medline]
Dietrich RA, Delaney TP, Uknes SJ, Ward ER, Ryals JA, and Dangl JL, 1994. Arabidopsis mutants simulating disease resistance response. Cell 77:565–577.[CrossRef][Web of Science][Medline]
Greenberg JT and Ausubel FM, 1993. Arabidopsis mutants compromised for the control of cellular damage during pathogenesis and aging. Plant J 4:327–341.[CrossRef][Web of Science][Medline]
Greenberg JT, Guo A, Klessig DF, and Ausubel FM, 1994. Programmed cell death in plants: a pathogen-triggered response activated coordinately with multiple defense functions. Cell 77:551–563.[CrossRef][Web of Science][Medline]
Hammons RO, 1973. Genetics of Arachis hypogaea. In: Peanuts-culture and uses. Stillwater, OK: American Peanut Research and Education Association; 135–173.
Hu G, Yalpani N, Briggs SP, and Johal GS, 1998. A porphyrin pathway impairment is responsible for the phenotype of a dominant disease lesion mimic mutant of maize. Plant Cell 10:1095–1105.
Johal GS, Hulbert S, and Briggs SP, 1995. Disease mimics of maize: a model for cell death in plants. BioEssays 17:685–692.[CrossRef]
Patil SH, 1966. Mutations induced in groundnut by X-rays. Indian J Genet 26A:334–348.
Patil SH, Kale DM, Deshmukh SN, Fulzele GR, and Weginwar BG, 1995. Semi dwarf early maturing and high yielding new groundnut variety, TAG-24. J Oilseeds Res 12:254–257.
Wolter M, Hollricher K, Salamini F, and Schulze-Lefert P, 1993. The mlo resistance alleles to powdery mildew infection in barley trigger a developmentally controlled defense mimic phenotype. Mol Gen Genet 239:122–128.[Web of Science][Medline]
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