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Saxena M.C. (ed.), Cubero J.I. (ed.), Wery J. (ed.).

Present status and future prospects of chickpea crop production and improvement in the Mediterranean countries

Zaragoza : CIHEAM

Options Méditerranéennes : Série A. Séminaires Méditerranéens; n. 9 1990

pages 55-60

Article available on lin e / Article dispon ible en lign e à l’adresse :

--- http://om.ciheam.org/article.php?ID PD F=91605011

--- To cite th is article / Pou r citer cet article

--- Crino P. Ch ickpea breedin g for resistan ce to Ascoch yta bligh t. In : Saxena M.C. (ed.), Cubero J.I.

(ed.), Wery J. (ed.). Present status and future prospects of chickpea crop production and improvement in the Mediterranean countries. Zaragoza : CIHEAM, 1990. p. 55-60 (Options Méditerranéennes : Série A.

Séminaires Méditerranéens; n. 9)

---

http://www.ciheam.org/

http://om.ciheam.org/

(2)

Chickpea breeding for resistance to ascochyta blight

CRINO

ENEA C.R.E. CASACCIA

DEPT. AGROBIOTECHNOLOGIES P.O. BOX 2400, O0100 ROMA A.D., ITALY

- by Ascochyta rabiei of

to of

is the most effective way of the pathogen but the knowledge of to

of

as useful tool

not of of

by of inoculum at low

on the dipping of of A. rabiei and

- “Amélioration du pois chiche pour la résistance à l’anthracnose”. L’anthracnose causée par

Lab. est des facteurs limitants de la production du pois chiche dans les conditions méditerranéennes, particulièrement lorsque la date de semis est avancée vers l’hiver. L‘utilisation de cultivars résistants est le moyen le plus sûr pour contrôler ce pathogène;

mais la connaissance des races d‘anthracnose est pré-requis très important pour tout programme de sélection. Afin d‘obtenir des lignées de pois chiche résistantes à l‘anthracnose, on a développé en depuis 1982 dlTérentes stratégies d‘amélioration:

évaluation de ressources génétiques locales ou internationales composées d‘espèces cultivées ou sauvages, ou croisement des lignées agronomiquement intéressantes avec les lignées résistantes. La mutagénèse a été utilisée pour induire de nouvelles résis- tances génétiques non disponibles dans la nature. Des méthodes permettant de cribler un grand nombre de lignées ont été développées en serre avec inoculation art$icielle, puis au champ en présence d‘inoculrcm à faible concentration. Cette dernière méthode est basée sur le trempage des graines d‘un témoin dans une suspension de conidies mises ensuite en culture alternée avec des lignées à tester.

Introduction

caused by Ascochyta rubiei is the

most disease of chickpea in

of

sowing

in when high humidity

epidemics. by the use of fungicides in such situations is inadequate. use of cul- is the only and effective way available up to date (Singh et al., 1984). of

identified in the last 50 (Table 1) but some- times the of new os A. rubiei has instance, cvs. F8 and

C 12-34 became susceptible. They substituted by the CV. C 235 obtained in 1960.

of Some of these

have

adapted and high yielding and some lines have been

few studies on the genetic of to ascochyta blight in the

ing a limitation chickpea

done so shows that the is by a

single dominant gene (Table 2). dif-

(3)

Table 1. Chickpea resistant cultivars released in' dif- ferent countries.

F8 C 12-34

c

235

C127 AYELET, Sovkhozuyi 14,

199, 1-13

"12, C44, AUG-480

NAY, ATUL

-

Spain

et al., 1938 Ahmad et al., 1949

Athwal, 1962 Asiz, 1972

and V i , 1974

Singh, 1978

et al., 1983 Singh and Saxena, 1987 Sigh,

et al., 1988

independently genes

by allelic tests and 1986).

of

published so indicate that a of stomata unit of leaf, stem as well as a small

of to ascochyta

(Ahmad, 1952; 1986). The

tion of malic acid as a cause of in F8 than in susceptible 1952) was not con-

by subsequent studies.

between and susceptible showed a

and catalase activity and L- cystines and phenolic content inoculation of the ones and 1974 a,b; 1975 b,c). A high level of phytoalexin and maackiain in

plants has by Weigand

et al. (1986). Studies on the of

to .phytoalexin also in

at Stazione di la

Sicilia in with ENEA and

tale la Vegetale of

Screening methods

pea in a of

both field an techniques has not

Table 2. of resistance to ascochyta blight in chickpea.

F10 1-13 Code no. 12-92

12, 200, 4935 191

M:

2w, 201 195, NEC 138-1

Gene Single dominant Single dminant Single dominant Single dominant Single dominant Sigle Sigle doniant

Hafiz

& Ashaf, 1953

Vi.

et al., 1975 1916 Sigh &

Sigh Açigàz, 1984 Açigàz, 1984

& 1986

& 1986

to The

attemps of

ly new Nene, 1979) and field

et al., 1980) have been

Also in and field techni-

developed in to test of

lines. the tests done in

(t=22+4"C) plastic 15-day old

seedlings with a suspension (1.8 lo5

ml-') of the fungus. The humidity is maintained at about 90% keeping the closed 5 days.

12-15 days, disease incidence is

to a 0-5 scale; the of individual classified as follows: 0-2.5 = 2.5-5 = sus- ceptible. This technique was also utilized the

of Ascochyta rabiei

established that 15 day old plants can give useful to the suscep- tibility of the tested lines at an inoculum

between 2 lo4

ml-'

and 2

lo5 ml-'

unpublished data; et al., 1987).

A technique field conditions and in sowing, was

et al., 1987). Some seeds of the susceptible line dipped one night in a conidial suspension of

A . rabiei and, in an oven with ventila-

tion, they between 2 single of the

to be tested. The lines following 1-9 scale by Singh et al. (1981). lines

the subsequent seasons assess- ment.

- 56 -

Serie A: Seminaires mediterraneens

(4)

Strategies of breeding

to ascochyta blight

almost 50 the selection of lines

the existing accessions and

has been done by the the develop- ment of blight lines with a

plant type, length of the biological cycle, cold

and seed size. supplied to

utilization in the national chickpea Evaluation of some wild species of Cicer

to

(Sandhu, 1980; Van 1984) but only few available indicating use in the

cific 1975; and

Van et al., 1987).

unsuccessful except the combination C. arietinum X C. reticulatum.

Some and chickpea

cated the use of mutation to a specific

in a without its

mutants to A. rabiei have been induced by gamma and chemical mutagen

at in et al., 1983) and

et al., 1988).

the of

to blight, by

FAO, was in 1975 in

1986). Significant between some suggested

tests and the field indicat-

ing a good estimate of in field. A

was at

as well in 1979-80 (Singh et al., 1984).

No the development of chick-

pea multilines due to little so available on physiological of A . rabiei (Singh et al., 1984).

Current research in Italy

the and of ascochyta

blight attacks one of the limiting

chickpea causing losses

of yield. to obtain lines, since 1982, 1)

ing and as well as local

by lines

with the ones. is utilized

the induction of new (against 6 of A . rabiei) not existing in the available ’gene pool’ (Fig. 1).

A wide collection of

(569 lines) (Table 3) was

Table 3. Number of germplasm lines evaluated at ENEA since 1981-82 to 1987-SS.

origin

Tunisia Unknown Spain

Analysed genotypes (No.)

235 86 59 35 31 19 10 9 7 6 6 5

Origin

Egypt USA

Afghanistan Yugoslavia Ethiopia Total

Analysed genotypes 4 4 4 3 3 3 3 3 2 1 569

to A. rabiei in field

conditions in and South

5 localities, 2

lines 72) showed a good

of high disease incidence

in open field. of additional

sowing, they have been in 1987 as “Sultano” and “Califfo” (Calcagno et al., 1988) and

they now adding to

list.

Among 280 lines tested ascochyta in

field 1987-1988, 174 lines (Table

4) including also 31% of F,, F6, F7 and F,

selected genetic as well as

ascochyta F4

at ENEA. Selected is also

being tested by inoculation with each of A.

rabiei, in to assess the type of With the aim to combine

with the

in 1984. F, has been multiplied in and then two

followed on F2 and F3 selection

in field and only selection

in the next the

lines obtained will be evaluated

then, in F6, F7 and F,, multilocation will be out (Fig.1).

some a of genes con-

the to ascochyta blight has been in the “Sultano” and “Califfo”. studies

to the data and to obtain

(5)

I

T

1

(200 m

hl3

inxulaticn men- hntse ru% 6)

1

J I - - -

Fig. 1. of to A . rubiei in

Table 4. Chickpea lines selected in field for resistance to ascochyta blight during 1987-88.

F5 F7

F6

Total

(No.) (No.)

10

10 14 12

31 38

2

122 112

9 6

67 7

2 1

11 -

280 174

-

Table 5. to ascochyta infection of some acces- sions of chickpea wild species coming from the regional plant introduction station of Washington State University (USA).

Vid species origin

Ethiopia Lebanon

Accessions 489171 458556 489176 458554 458550 458551 458558 458559

2.00 0.86 1

A.

S

S

S = susceptible; =

- 58 -

Serie A: Seminaires mediterraneens

(6)

on the of in lines.

Eight accessions of chickpea wild species coming

the Station of Washington

State analysed to

the 2nd of A. rabiei in field

conditions of infection (Table 5). could be useful to them against the most of A. rabiei

to the of into

the cultivated species. New techniques in should be developed to the incom- of to 6 objectives of a

ject in 1988 between and

A mutation has also

in 1986-87. 20 kg. of seeds of “Calia”

with gamma at the dose of 200 Gy.

a multiplication of in the field, inoculated with the 6 of A.

rabiei in The is still

but out of 5,000 plants, tested so 32

symptoms. studies field conditions in the past unsuccessful et al., 1987).

Conclusions

lines to ascochyta blight have been now in some chickpea collections. use may be limited by the existance of of the pathogen and, in this

should be on the

at

intensive is of stable

as well as the study of the and mechanism of to blight. The identification of

lines to each physiological as by

in this meeting could suggest the possible genes in the existing which could be into a single genotype.

The of new which does

not to be existing in the available neces- of

could also be usefully utilized but emphasis is the development of in vitro techniques A

between

ing on chickpea ascochyta blight is

References

(1984): Studies on of of

21 (2): 145-156.

A. and ings of

of 1:

18-22.

ASE, - a new

J. 165-166.

F.

in

Cicer species. Euphytica 36:

667-675.

the (9): 20-22.

CALCAGNO, F., F. (1988): Una

il cece. 24 Luglio 1988:

35-38.

F., G. and

di

in in

A. and

6: 59-61.

of

with plant yield and of ascochyta blight L.).

of chickpea.

51-59.

J.S. S. to

Ascochyta blight. 27: 643-645.

of

A. (1953): Studies on of

in 43: 580-

581.

in 42: 422-424.

in plants,

in

and

of chickpea, lentil, pea and cowpea.

(7)

of

of the blight disease 7 (2): 45-47.

Cicer arietinum. of

A.

in chickpea to ascochyta blight. Euphytica 35: 1007-1010.

Cicer. 2-3.

ing of 2: 13-15.

case induced muta- ings Symposium on

(Cicer

arietinum L.) to 13-

15.

of

disease, Ascochyta rabiei 59:

41.

Fonti genetiche di cece

nel bacino del La

and G.C. (1984):

of on

ing of Chickpea (Saxena, and Singh, eds.).

of

to ascochyta blight in 23: 9-10.

in chickpeas to Ascochyta rabiei 586-587.

of genetic stock against

J. 8: 124.

SOLEL, J. (1964): The of ascochyta

of 3: 119-120.

to ascochyta blight in chickpea (Cicer arietinum L.). Euphytica 211-215.

bility and use of wild Cicer 57: 19-24.

S., J.S. and GWTA,

in chickpea. Euphytica 24: 209-211.

S. J.S. (1975): Change in catalase activity of

by Ascochyta rabiei 28:

223-225.

S. J.S. of in

28: 206-208.

S. J.S. (1974): Changes in phenolic content plant induced by Ascochyta rabiei

27: 524-526.

S. J.S.

with ascochyta blight (Cicer urietinum L.).

13: 174-175.

J.,

(1986): Accumulation of phytoalexins and isoflavone glucosides in a of Cicer arietinum

with Ascochyta rabiei. J. 115: 214-221.

- 60 -

Serie A: Seminaires mediterraneens

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