Application of SSR markers for identifying resistance to ...shodhganga.inflibnet.ac.in/bitstream/10603/6096/15/15_chapter 7.pdf · resulting from chlorosis caused by CMD leads to

Identification of CMD and Whitefly using SSR

186

Chapter 7

Application of SSR markers for identifying resistance to

Cassava Mosaic Disease and White fly infestation in Cassava


187

Introduction

Cassava (Manihot esculenta Crantz) provides food to large number of small

and marginal farmers and also supplies raw material for cheaper starch and starch

products. As discussed in the introduction chapter the productivity and yield of

cassava is affected by many diseases and pests.

Among the different diseases, Cassava mosaic disease (CMD) is the main

biotic constraint in cassava production and the most important threat to food security

in sub-Saharan Africa (Thottappilly, 1992). Cassava mosaic disease (CMD) is caused

by any one or a combination of the cassava mosaic Begomo virus (family

Geminiviridae) transmitted by a vector, the white fly.

The genomes of most Gemini viruses are bipartite, termed DNA A and DNA

B, the former encodes functions associated with viral replication and encapsulation

and the latter encoding the movement functions (Harrison and Robinson, 1999). The

typical symptom of the disease and mode of transmission are explained in the

introductory chapter. Figure 7.1 shows a normal and cassava mosaic virus (CMV)

infected cassava plants in parallel. A typical CMV affected cassava leaf and the

causative vector, whitefly are presented in Figure 7.2. This disease is prevalent in all

cassava cultivating regions of Africa, Indonesia and India; meanwhile it is of

relatively rare occurrence in South America. In affected plants, the chlorosis varies

from almost 100% of leaf surface to less than 5%. Reduced photosynthetic activity

resulting from chlorosis caused by CMD leads to reduced tuberization and smaller

yields or no yield at all. The yield loss due to CMD ranges from 20-90%. Estimated

total crop yield losses due to CMD in Africa amounts to about US $ 440 million per

annum (Thresh et al., 1997).


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Figure 7.1: Normal (left) and CMV infected (right) cassava plants

Figure 7.2: White fly infestation on cassava leaf (left) and white fly (right)

CMD is a viral disease caused by at least seven different Gemini viruses viz.,

African cassava mosaic virus (ACMV), the East African cassava mosaic virus

(EACMV), Ugandan Variant of Eacmv (ugA), South African cassava mosaic virus

(SACMV), Madagascar cassava mosaic virus (MCMV), Indian cassava mosaic virus

(ICMV) and SriLankan cassava mosaic virus (SLCMV) (Malathi et al., 1987; Hong et


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al., 1993; Geddes, 1990; Zhou et al., 1997; Thresh et al., 1998). All these viruses are

transmitted by the whitefly, Bemisia tabaci to an extent of 5 percent only.

Fauquet and Fargette (1990) have identified six different components of

resistance to CMD, such as field resistance (percentage of infected plants), vector

resistance (number of adult whiteflies per plant), inoculation resistance, virus

resistance, symptom severity, and virus diffusion resistance (development of

symptoms over time). The disease is best kept under control by the deployment of

resistant varieties (Thresh et al., 1997). The studies conducted by Hahn et al., (1980)

indicated the possibility of several genes responsible for resistance. Akano et al.,

(2002) reported that the resistance could be due to a major dominant gene (CMD2) by

using Nigerian landraces.

Resistance to CMD was first obtained from a cross between cassava and its

relative Manihot glaziovii Muller Von Argau (Nicholas, 1947). After three

backcrosses into cassava to obtain suitable storage roots, the clone 58308 was

selected, and for decades this clone and its derivatives have been extensively used as

the main source of resistance in breeding for resistance to the disease. This has

resulted in the selection of several improved cultivated cassava genotypes of the

Tropical Manihot Selection (TMS) series, with resistance to CMD (Hahn et al., 1989).

Some African landraces, the Tropical Manihot Esculenta series (TME), collected in

West Africa have also been identified to be resistant to CMD (Mignouna and Dixon,

1997) and could serve as alternative sources of resistance to increase the genetic base

of resistance to the disease.

A study on the inheritance of resistance to CMD in some of the African

landraces has revealed polygenic and recessive inheritance with susceptible

accessions also contributing to resistance (Lokko et al., 1998). Hahn et al, (1980)


190

inferred from the polygenic mode of inheritance that resistance to the disease must be

attributed to the combined action of a number of loci, which are linked as a

chromosome, or a set of chromosomes in a genome. Population improvement and

recurrent selection were therefore recommended in breeding for resistance to the

disease.

Quantitative genetic analysis has also shown allelic differences and

complementarity of genes for resistance to CMD in the African germplasm (Lokko et

al., 2005). Akano et al, (2002) suggested that there could be different mechanism of

resistance to CMD in cassava genotypes. An understanding of these resistant

mechanisms will be useful in breeding efforts particularly in marker assisted selection

(MAS) programmes. The detection of multiple genes for virus resistance using

segregation analysis alone is not efficient because of the confounding effect of the

environments and its interaction with the genotype (Mc Mullen and Louie, 1989). The

expression of CMD in different cassava genotypes is known to be dependent on the

environment, and there is a strong relationship between the range of symptoms

produced and genotype x environment interaction (GXE) (Fargette et al., 1994).

Hence molecular marker analyses are suitable for such studies. Marker systems such

as Isozymes, RFLPS, RAPDs, SSRs and ESTs have been used to develop a cassava

framework map consisting of two geographic divergent parents (Fregene et al., 1997).

The two strategies frequently used to identify molecular markers associated with traits

of interest include genetic linkage mapping and bulk segregant analysis (BSA)

(Michelmore et al., 1991; Tanksley et al., 1989; Giovannoni et al., 1991). Akano et

al., (2002) used BSA of land races to identify a SSR marker linked to another CMD

resistance gene, designated CMD2. To date two CMD resistance genes CMD1 and

CMD2 have been placed on the map (Fregene et al., 2001; Akano et al., 2002).


191

Among the different control measures suggested for CMD, the most promising

one is the use of CMD resistant varieties. Other control measures suggested include

the careful selection of planting material, controlling the vector, whitefly and

inactivation of the virus through heat treatment. Therefore breeding varieties of

cassava having resistance to CMD is highly important and screening of germplasm

and available varieties is a prerequisite for identifying the same.

Indian Cassava Mossaic Disease (ICMD) is a serious constraint to cassava

production in India. This disease is reported to be widespread in South India mainly

in Kerala, Tamil Nadu and Andhra Pradesh (Narasimhan and Arjunan, 1976). Yield

losses up to 88% in highly susceptible cultivar ‘Kalikalan’ and 17 to 36 per cent in

improved varieties released by CTCRI were reported (Malathi et al., 1985). The

symptoms of CMD are identical in Africa and India. Two disinct begomoviruses, viz.

Indian cassava mosaic virus (Hong et al., 1993) and Sri Lankan cassava mosaic virus

(Saunders et al., 2002) cause CMD in Asia. Complete nucleotide sequencing of two

cloned ICMV DNAs, one from the southern state of Kerala (Hong et al., 1993) and

another from the central state of Maharashtra (Saunders et al., 2002) showed that they

were highly similar to each other, indicating them to be isolates of the same virus. In a

PCR-RFLP study to analyze the genetic diversity of geminivirus associated with

CMD, it was found that both ICMV and SLCMV were present in mosaic-affected

cassava; ICMV was geographically restricted to certain regions, whereas SLCMV

was widespread (Patil et al., 2005).

In the germplasm maintained at CTCRI most of the accessions are found to be

susceptible to CMD and white fly infestation. However a few of them were found to

be phenotypically symptom free. But, among the symptom free accessions, a number

of varieties succumbed to the disease over the years. Therefore, there is an urgent


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need for a more reliable approach for screening for CMD resistance. In view of this

the objectives of the present study includes-

(1) Screening of selected cassava varieties (phenotypically resistant varieties,

susceptible varieties and hybrid varieties) for CMD and white fly

resistance using SSR markers.

(2) To find any relation between white fly infestation and CMD among

selected Indian cassava cultivars using SSR markers.


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Materials and Methods

Selection of plant material:

Three different sets of cassava plants were selected for the present study. Among the

1600 accessions of cassava available at CTCRI germplasm collection, 15 CMD

symptom free varieties constituted group one (Table 7.1). The second group consisted

of 15 varieties, also from the CTCRI collection, but susceptible to CMD (Table 7.2).

The third group consisted of 45 interspecific hybrid varieties (Table 7.3), which

include both CMD resistant and susceptible varieties.

Sl. No Varieties Sl. No Varieties Sl. No Varieties

1 Ce-144 6 Ce-273 11 Ci-800

2 Ce-594 7 Ce-97 12 Ce-85

3 Ce-28 8 Ce-547 13 Ce-28

4 Ce-347 9 Ce-152 14 Ce-195

5 Ce-218 10 Ce-185 15 Ce-391

Table 7.1: List of 15 CMD symptom free accessions

Sl. No Varieties Sl. No Varieties Sl. No Varieties

1 CE-152 6 CE-33 11 CE-308

2 CE-185 7 CE-166 12 CE-38

3 CE-39 8 CE-82 13 CE-348

4 CE-180 9 CE-96 14 CE-785

5 CE-279 10 CE-301 15 CE-58

Table 7.2: List of 15 CMD susceptible varieties


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Sl. No Variety Susceptible/

Resistant

Sl. No Variety Susceptible/

Resistant

1 GD13 Semi resistant 24 CR45 do

2 G214 Resistant 25 CR52A do

3 G196 Resistant 26 CR43 do

4 G120 Resistant 27 CR59 do


6 TCH-1 Susceptible 29 CR53A do

7 MNGA 1 Resistant 30 CR36 do




11 CI732 Susceptible 34 CR43 do


13 GKOD2 Recoverable 36 MNGA S 2-1 Resistant

14 G136 Resistant 37 MNGA S 2-2 Resistant

15 CMR4 Recoverable 38 MNGA S 2-3 Susceptible

16 CR43 Resistant 39 MNGA S 2-4 Resistant

17 CR41 do 40 MNGA S 2-5 Resistant


19 52A do 42 MNGA S 2-7 Resistant




23 CR54A do

Table 7.3: CMD resistance/susceptible nature of 45 inter-specific hybrids varieties

Characterization of tuber:

Tubers were collected and weighed by weighing machine for each accession. After

cooking the tuber the cooking quality was checked by organoleptic method.

Identification and counting of Whitefly:

Whiteflies were counted using hand lens.


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SSR variability analysis:

Extraction of DNA, PCR and Electrophoresis:

Approximately 100 mg fresh leaf samples were used for extracting the DNA from all

the plants selected. The details of DNA extraction is already presented in Chapter 3.

SSRY Markers and PCR amplification:

The details of primers used in the study are consolidated in Table 7.4. The

amplification was performed in a thermal cycler (MJ Research PTC-100, USA). The

master mix (25µl) containing 50 ng genomic DNA, 1.0X Buffer 10X (500 mM KCl,

100 mM Tris-HCl pH 8.8,Tritón X-100), 1.5mM MgCl2 (25mM), 0.1 mM dNTPs

(2.5mM), 0.2uM each primer (10uM) y 1.0 U Taq polymerase. Denaturation step of 2

min at 95 °C followed for 30 cycles, and each cycle consisted of a 30s denaturation at

94°C, 1min annealing at 55 °C, and 1min extension at 72°C. The last step is consisted

of additional extension of 5min at 72 °C.

Primer Sequence (5'……3') Target Product size

SSRY 28F TTGACATGAGTGATATTTTCTTGAG CMD 180 bp

SSRY 28R GCTGCGTGCAAAACTAAAAT

SSRY 234F TTGCCAGAACCCTAGGAGTAA Whitefly Resistance

196 bp

SSRY 234R TGTCCCTAGGAAGGTTGCTG

Table 7.4: Details of primers used in the study including target


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Results

The fifteen CMD symptom free accessions (Table 7.1) screened in this study, the

incidence of whitefly infestation (in the form of pupae, nymph and adult male/female)

was found in varying intensities (Table 7.5). Similarly the fifteen CMD susceptible

varieties (Table 7.2) also exhibited difference in whitefly infestation (Table 7.6). The

morphological features of the 45 interspecific hybrid varieties studied are

consolidated in Table 7.7. Among the 15 accessions screened for CMD and whitefly

SSR markers, only one accession (CE 273) was found resistant (lane no. 8 in Figure

7.3).

Sl.

No

Accession

No.

Number of

Pupae Nymph Female

fly

Male

fly

Total

white fly

1 CE-144 0 8 0 0 8

2 CE-17 3 11 0 0 14

3 CE-594 5 13 0 0 18

4 CE-28 11 15 2 1 29

5 CE-347 17 22 3 0 42

6 CE-218 5 46 3 0 54

7 CE-273 12 27 16 6 61

8 CE-97 27 32 2 0 61

9 CE-152 3 68 3 0 74

10 Ci-800 7 61 6 1 75

11 CE-185 8 92 5 0 105

12 CE-547 10 128 4 1 143

13 CE-195 13 141 8 2 164

14 CE-391 17 196 3 0 216

15 CE-85 15 245 7 0 267

Table 7.5: Number of pupae, nymph and adult whitefly present in 15 varieties of phenotypically CMD resistant varieties of cassava.


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Sl.

No

Accession

No.

Number of

Pupae Nymph Female

fly

Male

fly

Total white

fly

1 CE-152 0 5 1 0 6

2 CE-185 8 409 21 8 446

3 CE-39 0 24 1 0 25

4 CE-180 1 154 2 2 59

5 CE-279 5 157 9 1 172

6 CE-33 10 106 2 2 120

7 CE-166 19 161 6 0 186

8 CE-82 5 36 12 4 57

9 CE-96 6 13 0 0 19

10 CE-301 3 42 0 0 45

11 CE-308 8 248 9 0 265

12 CE-38 11 49 12 3 75

13 CE-348 6 45 4 1 56

14 CE-785 5 418 7 3 433

15 CE-58 3 37 5 0 45

Table 7.6: Number of pupae, nymph and adult whitefly present in 15 varieties of CMD susceptible varieties of cassava. The CMD free accession (CE 273) also showed positive result for the presence of

whitefly resistance as shown in Figure 7.4.


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Name

Plant

Type

Stem

color

Petiole

color

Shape

of

central

leaf

Tuber

Shape

Tuber

skin

color

Rind

color

Flesh

color

Neck

Flowering

MNGA S 2-1 NB SGY G LA CY C PI W S F

MNGA S 2-2 NB LB G E CO B C W L F

MNGA S 2-3 TB LB R L CO C C C L F

MNGA S 2-4 SSP GR G LE CO LB LPI C S F

MNGA S 2-5 MB G PI L CY LB LPI C S F

MNGA S 2-6 TB B G E CO LB LY C S F

MNGA S 2-7 TB B G L CY LB C C S F

MNGA S 2-8 NB B PI L CY B LPI W S F

MNGA S 2-9 NB SGY G L CO LB C W S F

MNGA S 2-10 TB SGY G LE CY LB C C S F

CR 43-7 SSP RB P E CY LB C W L NF

CR 41-2 SP GY G L LCY LB C C L

CR 35-18 TB B DP L CO B C C S -

CR52A -43 SSP GY G E LCY B C W S F

CR44-6 SSP SGY LP L CY B PI C S -

CR43-2 NB B PG E CO LB C C S -

CR36-2 NB GY P LE CY B PI W S -

CR 54A-43 TB DB LG L CY B C C S F

CR45-9 TB CGY P L CO B Y C S -

CR52A-4 TB GY G E CY B OY C S -

CR43-11 TB B P L CO LB C C S SF

CR59-8 TB GY C L LCY LB C W S F

CR20A-2 NB GY DP L LCY PI C C L -

CR52A-19 TB GY G LE CO B C C S -

CR36-2 NB GY P E CO B PI W S -

CR52A-26 TB GY LG L LCY B C C S -

CR26-2 NB GY P L CO LB PI C S -

CR41-2 SSP GY G L CO LB C C S -

CR43-6 TB GY LG E LCY LB PI C S -

CR43-14 SSP DB P/G LA CO LB C C S -

GD13 NB GY PI E CO B LPI C S F

G214 NB B G L CO B C W S F

G196 TB GY G L CO LB C C S F

G120 SSP SGY PI L CY B C C S F

G355 SP B G LE CO B C W S F

TCH-1 TB GY G E CY B C C S F

MNGA 1 TB GG DG L LC SW W W A F

G104 SSP CGY G L CO LB PI C L F

GD15 NB GY DP E CY LB C C L F

GD16 NB B G L CY PI PI W S F

CI732 TB GY LP L LCY B C C S NF

GD86 TB GY PG L CO B Y C S

GKOD2 TB GY P LE LCY B OY W S -

G136 TB GY LG E CY B C C S F

CMR4 TB GY P L CO LB C W S -

NB:Non branching; TB: Top branching; SSP: Semi-spreading; SP: Spreading, SGY:Silver grey;GY:grey; G:Green;B:Brown; RB:Reddish brown; LB: Light brown; DB: Dark brown, GY: Greyish yellow, PI:Pink, P:Purple, LG: Light green, DP: Dark purple P/G:Purplish green, La: Lanceolate, E: Elliptical; LCY: Long cylindrical, CY: Cylindrical, Co: Conical, ,Y: Yellow,C:Cream,

Table 7.7: Morphological details of the 45 interspecific hybrids studied.


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Figure 7.3: Gel image showing CMD resistant marker in the variety CE-273 (lane no. 8); Lane M showing 1kb molecular weight marker (Electrophoresis conditions: 1.2% agarose, 2 hrs, 80V).

Figure 7.4: Gel image showing white fly resistant marker in the variety CE-273 (lane no. 15); Lane M showing 1kb molecular weight marker (Electrophoresis conditions: 1.2% agarose, 2 hrs, 80V).

Among the 15 CMD susceptible varieties screened, none of them gave positive results

either for CMD resistance or for whitefly resistance. Meanwhile, among the 45

interspecies hybrid varieties screened, a single genotype (MNGA1) showed positive

result for CMD resistance (Figure 7.5). However, screening for whitefly resistance

resulted in negative result among all these varieties.


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Figure 7.5: Representative gel image showing CMD resistant marker in the variety MNGA (lane no. 14); Lane M showing 1kb molecular weight marker (Electrophoresis conditions: 1.2% agarose, 2 hrs, 80V).

The symptom free accession (CE-273) also showed highest tuber yield (39.5 T/Ha),

total protein content (45.53## on dry weight basis) and “Good” cooking quality. A

comparison of tuber yield and cooking quality of CE-273 and few randomly selected

accessions are given in Table 7.8.

Table 7.8: Tuber yield and cooking quality of Ce-273 and few randomly selected varieties from CTCRI cassava collections.

Among the interspecies varieties screened, the CMD resistant variety MNGA also had

“Excellent” cooking quality.

Sl.

No

Acc. No Tuber yield

(t/ha)

Cooking

quality

1 Ce-273 39.50 Good

2 Ce-152 37.03 Good

3 Ci-96 34.57 Medium

4 Ce-82 30.00 M 5 Ce-58 28.39 M

6 Ce-17 28.39 M

7 Sree Vishakam 24.69 M

8 M4 Std 20.98 Good


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Discussion

The normal screening practice for CMD and whitefly resistance is time

consuming and not reliable. On the other hand the present study based on SSR marker

provided more reliable and reproducible results. Since CMD was identified as crucial

in determining the yield/productivity in cassava, researchers have been searching for

resistant varieties through different approaches. The most rewarding programmes to

find CMD resistant varieties began in Tanzania during the late 1930s and later in

Madagascar, where all local varieties and many diverse cassava accessions were

screened (Cours-Darne, 1968; Jennings, 1994). Continuous CMD epidemics and

extensive introductions of bred varieties through out the country with the replacement

of local varieties will most likely further reduce the genetic diversity (Kizito et al.,

2005). It is found out that in India, field-grown cassava contains both ICMV and

SLCMV, displaying high variability (Patil et al., 2005).

Considerable progress has been made in developing a comprehensive

molecular genetic map and a clustering of cassava accessions into groups having

differential resistance (Fregene et al., 1997; 2001). Furthermore, progress has also

been reported in localizing resistance genes (Akano et al., 2002). This provides

opportunity to apply marker-assisted breeding for efficient selection of this trait. The

SSR marker based method can be used for screening of symptom free hybrids at

seedling stage itself.

Host plant resistance was developed through crossing cultivated cassava with

wild relatives like M. glaziovii. In resistant varieties, plants may recover a

phenomenon in which newly emerging leaves of an infected plant sprout without

symptoms. Studies showed that restriction of virus movement into axillary buds is an

important aspect of resistance in CMD (Ogbe et al., 2002). It was also speculated that


202

inhibition of long distance transport of virus plays a critical role. Once a leaf becomes

infected, the virus spread effectively from cell to adjacent cells but not to other leaves.

Therefore it appears that cell to cell movement is not inhibited and the recessive gene

affects long distance transport of the virus (Thottappilly et al., 2003).

The gene controlling resistance to the M. glaziovii (tree cassava) source of

resistance has been designated CMD1. Although highly resistant varieties of this type

are available in many countries, they are not always widely grown due to the lack of

adequate quantities of planting material and in many countries farmers continue to

grow local varieties including some that may have little or no resistance to CMD

(Thottappilly et al., 2003).

In resistant genotypes, cuttings obtained from the lower portions of the main

stem are more likely to grow into virus-infected plants than cuttings from the upper

portion of the main stem and stem branches (Cours, 1951; Njock et al., 1994).

Among the screened varieties in the resent study, CE-273 which was CMD

resistant positive was found to have good yield and good cooking quality as well. This

could be attributed to the healthy nature of plant with more photosynthetic activity.

The total number of white fly is 61 (including pupae, nymph and adults). Whereas,

varieties CE-144, CE-17, CE-594, CE-28, CE-347 and CE-218 (all CMD resistant)

having lesser number of white fly than CE-273, did not showed marker for CMD

resistance. Also, among the CMD susceptible accessions, CE 152 has also white fly

numbers less (6 nos.) compared to CE-273 (61 nos.). These results show that the

white fly can even infest CMD resistant plant and number of white fly could not

considered as a monitoring/assessing criteria for CMD resistance in cassava. In other

words resistance to virus infection differs from resistance to the whitefly vector.

Palaniswami et al., (1996) have reported that extent of spread of ICMV by the


203

whitefly Bemisia tabaci varies in field. Studies have also observed spread through the

vector is very low in improved cultivars (Chacko and Thankappan, 1973; Hrishi et al.,

1977). Whether this low spread is due to the field resistance of these varieties or due

to the inefficiency of the vector, is not clearly understood. It was also reported that

only cassava biotype of B. tabaci transmit ICMV (Palaniswami et al., 2004).

Fargette et al., (1996) have observed cassava genotypes differed widely in

whitefly infestation. Similar number of whiteflies on resistant and susceptible

genotypes had been reported by Hahn et al., (1980). He had also found that

populations of whitefly vectors vary frequently with variable environmental

conditions such as rainfall distribution, light intensity and temperature; thus, field

evaluation for CMD-resistance screening that relies on vector-transmission of the

virus can be unpredictable and non reliable. On contrary, few studies have shown a

correlation between whitefly population and disease incidence (Leuschner, 1977;

Otim-Nape et al., 1998). In a different study, a variation in the suitability of cassava

as a host for B. tabaci has been reported (Legg, 1994). This could be exploited in

breeding for resistance to the vector. The presence of the virus in some of the

resistant samples suggests that field resistance observed as symptoms, was not

necessarily an indication of resistance to virus infection. It was also suggested that

CMD evaluation requires evaluation tests in multiple environments to confirm the

resistant genotypes (Lokko et al., 2005). Using field evaluation, axial bud inoculation

and PCR, concluded that field resistance as shown by lack of symptoms was not

necessarily an indication of resistance to virus infection, but could be partly due

to lack of virus multiplication (Ogbe, 2001). The A genome of Gemini viruses of

which the cassava mosaic viruses belong, encode a protein required for their

replication and must recruit the remaining DNA replication mechanism from the host


204

plant, while the B genome is responsible for spread and symptom production

(Estessami et al., 1991; Fontes et al., 1992). Since DNA replication is part of the

natural growth and development, it is possible that the virus is able to replicate

and probably even spread in the resistant plant but the subsequent disease symptoms

are inhibited.

The variety MNGA1 (Table 7.3) was found CMD resistant in this study was

the first CMD resistant line introduced to India. The evolution of CMD resistance

accessions in cassava is a result of random genetic drift (Lokko et al., 2006). During

the last four decades of research at CTCRI (the prime institution engaged in cassava

breeding in India), a large number of cassava varieties with varying reaction to ICMV

have been released (Nair et al., 1998). CTCRI has a rich collection (1638) of

indigenous (854) and exotic (784) cassava germ plasm (Pillai et al., 2004) of which

only 113 accessions were found be free from ICMD. Cassava variety MNGA1 and

Manihot caerulescence were identified as resistant to ICMV (Unnikrishnan et al.,

2002; Sheela et al., 2002). MNGA1 is a breeding line from IITA, designated as

TMS3001, received in 1994, which is having long cylindrical tuber and silvery white

skin colour. It had been continuously evaluated for CMD for the past 10 years and

showed 0 to 1% infection at field level while other lines exhibited 3 to 67% infection

(Unnikrishnan et al., 2002). Identification of mosaic disease tolerant/white fly

tolerant lines will speed up the breeding program, making it less costly. The use of

resistant cultivars, production and distribution of healthy planting material, improved

cultural practices and eventually strategic use of transgenic crops could provide more

sustainable solutions to cassava virus problems.


205

References

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