Journal of Agricultural Science (2002), 139, 4753.

# 2002 Cambridge University Press

DOI: 10.1017\S0021859602002241 Printed in the United Kingdom
47
Inheritance of resistance to Mal de R!o Cuarto (MRC)
disease in Zea mays (L.)
M. A. DI RENZO"*, N. C. BONAMICO", D. D. DI; AZ#, J. C. SALERNO#, M. M. IBANM EZ" :Nb
J. J. GESUMARIA"
" Facultad de AgronomTa y Veterinaria, Universidad Nacional de RTo Cuarto, Agencia nm 3, 5800 RTo Cuarto,
Argentina
# Instituto de GeneTtica Ewald A. Favret , Instituto Nacional de TecnologTa Agropecuaria, cc 25,
1712 Castelar, Argentina
(Revised MS received 2 May 2002)
SUMMARY
No genetic estimates for resistance to Mal de R!o Cuarto (MRC) disease in Zea mays (L.) are
currently available in the literature. Therefore, the objectives of this investigation were (i) to estimate
the variance and heritability of partial resistance to MRC disease and of other agronomic traits from
maize families and (ii) to examine associations among MRC disease severity values across dierent
environments and between MRC and other agronomic traits. These estimations, obtained in an
endemic area, could contribute to the design of ecient enhancement programmes and evaluation
activity for the improvement of MRC resistance. The research was conducted by testing 227 F
$
derived-lines from a cross between a susceptible dent line, Mo17, and a partially resistant int line,
BLS14, for MRC disease at two R!o Cuarto locations in each of 2 years. The resistance of the lines,
measured with a disease severity index (DSI), was normally distributed across environments.
Genotypic variances were highly signicant on all scoring environments. Estimates of genotype
environment interaction were also signicant, suggesting that certain genotypes have little stability
over dierent environments. For disease severity index all estimates demonstrated moderate
heritabilities ranging from 0n44 to 0n56 and were similar when based on individual environments or
across environment. Condence interval widths ranged from 34n88 to 50n30% as large as the
heritability point estimate. The correlations between environments were small enough to indicate that
families did not rank similarly in individual environments for MRC resistance. Disease severity index
correlated signicantly (P0n01) with plant height, leaf surface, leaf border, leaf length and tassel
type. Heritability estimates for plant height and tassel type were 0n48 and 0n38 respectively and for the
various leaf traits heritability values were very low. On the basis of the substantial genotype
environment interaction and the little association between DSI values in the dierent environments,
selection for an increased resistance to MRC disease would require evaluation of germplasm across
multiple years and locations. Tassel type would be a useful predictor of DSI and can be used
eectively to improve screening procedures.
INTRODUCTION
In Argentina, Mal de R!o Cuarto (MRC) is the
most important viral disease of maize (Zea mays L.),
which causes increasing damage to susceptible culti-
vars and accounts for yield losses of around 70% in
the years of greatest incidence (Lenardon et al. 1998).
The disease, which is caused by a member of the
family Reoviridae, belonging to the genus Fijivirus
(Bradfute et al. 1981; Nome et al. 1981; Marzachi et
* To whom all correspondence should be addressed.
Email : mdirenzo!ayv.unrc.edu.ar
al. 1995), occurs mainly in the R!o Cuarto county
(province of Co! rdoba), the rural areas near Chaja! n,
Sampacho and Suco being the most aected (March
et al. 1995). The MRC virus is naturally transmitted
in a persistent, propagative manner by the plant-
hopper Delphacodes kuscheli Fennah (Homoptera:
Delphacidae) (Remes Lenicov et al. 1985; Ornaghi et
al. 1993). Weed and cultivated gramineae such as
oats, wheat and rye constitute virus reservoirs and
host for populations of the vector (D. kuscheli). When
these cereals begin to senesce, the planthopper vector
migrates to neighbouring young maize plants
(Ornaghi et al. 1993). Highest levels of disease
48 x. :. bi rrNzo ET AL.
incidence and severity grades correspond with in-
fections at the coleoptile to one-leaf stage (Ornaghi et
al. 1999).
Insecticides such as the pyrethroids group can
reduce disease severity. However, genetic resistance
may achieve the most economical control of this
disease. Improved disease-resistant germplasm may
provide economically protable disease control and
an eective way of both increasing and stabilizing
production in aected areas. Partial resistance is a
breeding objective in many maize improvement
programmes; however, the development of optimal
breeding strategies has been limited by the little
knowledge about the inheritance of resistance to
MRC disease. Although disease resistance in maize is
frequently considered to be simply inherited, several
resistance traits have been found to be governed by
multiple genetic factors (Stuber 1995). Heritability
estimations would improve the eciency of germ-
plasm enhancement programmes by providing an
indication of the degree of genetic control for traits of
interest. Estimates of heritability for a trait are
derived from phenotypic values that are, in part,
inuenced by types of genic action, gene frequencies
and environmental eects. Thus estimates of heri-
tability are nested in the environment in which
measurements are made (Falconer & MacKay 1996).
Breeding for resistance to MRC disease, which is a
complex character, has been laborious and time
consuming. Although no maize genotypes completely
resistant to MRC have been identied, some have
partial resistance. Little is known about what pro-
portion of the resistance in the eld is the result of
genotypic, environmental or genotypeenvironment
interaction eects. Severe outbreaks occur when there
is coincidence of abundant natural virus reservoirs,
high densities of the vector migrants and a susceptible
stage in the susceptible cultivars (Harpaz 1972; Conti
1976a, b, 1984). When disease in the eld is analysed,
MRCresistance often proves to be a partially recessive
trait and not inuenced by extranuclear components
(Presello 1993; Presello et al. 1995). To contribute to
the breeding eorts for MRC resistance, we carried
out this study which attempts to (i) estimate the
variances and heritability of partial resistance to
MRC disease and of other agronomic traits from
maize families and (ii) examine associations among
MRC disease severity values across dierent environ-
ments and between MRC and other agronomic traits.
These estimations, obtained in the endemic area,
could be helpful to contribute to the design of ecient
enhancement programmes and evaluation activity for
the improvement of MRC resistance.
MATERIALS AND METHODS
Plant material and observations
Two inbred lines, Mo17, a dent line susceptible to
MRC disease and BLS14, a int line with partial
resistance to MRC, were used as parents. An F
#
population of 227 individuals originating from three
randomly chosen F
"
plants were selfed to produce F
$
derived-lines. The F
$
derived-lines were evaluated in
eld experiments during the summer cycle of 1999 at
the Sampacho and Bulnes location (SA99, BU99) and
during the summer cycle of 2000 at the Sampacho
(SA00) location only. Sampacho (33m 19h S, 64m 42h
W; 510 m elevation, 676 mm annual rainfall) and
Bulnes (33m 30h S, 64m 41h W; 433 m a.s.l., 671 mm
annual rainfall) locations, which have a soil type udic
Haplustolls, are located in the endemic disease area
from the temperate semi-arid region (R!o Cuarto
department, Argentina). Each yearlocation combi-
nation was treated as an environment.
Each experiment included 239 entries: 227 F
$
families, six entries of Mo17 and six of BLS14 used as
parental controls. These parental controls were not
included at Bulnes in 1999. The experimental design
was a randomized complete block design with two
replications of single-row plots 0n7 m apart and 3n0 m
long. Plants were thinned to a distance of 0n15 m. As
part of the experimental protocol the MRC infection
was natural. At Sampacho in 1999 and 2000 the maize
experiments were established in the same plot area
following a rotation with a winter oat crop. Disease
scoring was measured beginning 6070 days after
seeding (initial male owering). Plots were scored for
disease severity based on the rating system of Ornaghi
et al. (1999). Ten to fteen plants in the centre rows of
a plot were individually rated on a scale of 0 to 3. The
following disease grades were established: 0 lno
symptoms; 1 lmild symptoms: presence of galls on
the abaxial side leaves or enations; 2 lshortened
superior internodes, enations and hockey pole ears;
3 lsevere dwarng, enations and small ears with few
or no kernels. A disease severity index (DSI) based on
disease grades was calculated for each plot and used
to rate F
$
families for their resistance to MRC
according to Grau & Radke (1982) :
DSI l

(gradeinumber of plant in class)

i100\3itotal number of plant
The DSI has a range from 0 for no diseased plants
rated to 100 for severely diseased plants rated.
Other traits collected on initial male owering
include plant height measures and ratings of leaf
surface, leaf border, leaf length and tassel type. Plant
height (in cm) was measured as the distance from soil
level to the lowest tassel branch. Traits scored visually
were evaluated and rated as leaf surface (0: normal v.
1: folded) ; leaf border (0: normal v. 1: serrated) ; leaf
length (from 0: normal to 3: shortened) ; tassel type
(from 0: normal to 11: deformed and totally sterile).
Resistance to viral disease in maize 49
Data analysis
The ShapiroWilks statistic in PROCUNIVARIATE
of SAS (SAS Institute 1990) was used to test the null
hypothesis that the DSI ratings and the other traits
data of lines in the population were normally
distributed for each environment and across environ-
ments. A level of P0n05 was used to test for lack of
t. Because no signicant association between family
means and variance was observed, a transformation
of the DSI and plant height values was unnecessary.
The leaf surface, leaf border, leaf length and tassel
type ratings were transformed to square root (yj0n5).
Analysis of variance was conducted on the eld
data using PROC GLM of SAS. The analyses for F
$
derived-lines and environments were analysed as
random eects for each trait separately. Estimates of
variance components and broad-sense heritabilities of
traits were calculated on an F
$
family mean basis for
each environment and across environments. Estimates
of variance components, including genotypic variance
(#
g
), genotypeenvironment interaction (#
ge
) and
residual (#
e
), were calculated by equating the mean
square to their expected values. Following Hallauer &
Miranda (1981) a broad-sense heritability estimate
based on variance component was calculated for each
environment by:
h# l(#
g
)\[(#
g
)j(#
e
\r)]
and across environments by:
h# l(#
g
)\[(#
g
)j(#
ge
\l )j(#
e
\lr)]
where l and r denote the number of environments and
replicates within environment respectively.
Two-sided 90% condence intervals were also
computed to determine the precision of heritability
estimates. The 90% condence limits for h# were
dened using
1k[F

/
#
:df
"
,df
#
\F]
where Fl(1k h#)

" (Knapp et al. 1985).

Simple correlations coecients were calculated to
compare the mean DSI ratings of F
$
derived-lines
across three environments of endemic area and to
compare DSI ratings with plant height measures and
other trait ratings (leaf border, leaf surface, leaf
length and tassel type).
RESULTS
Although the three environments were naturally
infested, a large range in disease reaction was observed
across all 227 F
$
derived-lines indicating high infection
levels at all environments. However, the F
$
families
showed no consistent trend over the three environ-
ments because the mean was not similar for each
environment. The reaction of F
$
families was dierent
since the damage was most severe in both Sampacho
1999 and 2000 and less severe in Bulnes 1999 (Table
1).
The partially resistant parent, BLS14 exhibited less
disease than Mo17, the susceptible parent. This
dierence was highly signicant (P0n01) at
Sampacho in 1999 or 2000 and across environments
for the means of the data combined (Table 1).
Signicant variation occurred for reaction to MRC
disease among F
$
families. Mean rating of DSI on the
F
$
derived-lines exhibited near-normal distributions
in the separate environments and across environments
(Fig. 1). The average of F
$
family means was not
signicantly dierent (P0n05) from the mean of the
high parent Mo17 in every case. The continuous F
$
phenotypic distribution exhibited ranges that ex-
ceeded the range of the parental genotypes since some
of the F
$
lines were more resistant than BLS14 and
others were more susceptible than Mo17. There was
signicant (P0n05) transgressive segregation for
reaction to MRC disease with lines from F
$
having
greater disease than Mo17, although few lines from
F
$
had signicantly greater resistance than BLS14 in
any environment or across environments.
Estimates of genotypic variances (#
g
) were reliable
as reected by their small standard errors and were
highly signicant (P0n01) for MRC resistance on
all scoring environments (Table 2). Estimates of
genotypeenvironment interaction (#
ge
) were also
signicant for the data combined over all environ-
ments, and fourfold greater than the genotypic
variance. These results suggest that certain genotypes
are less stable over dierent environments.
All estimates demonstrated moderate heritabilities
ranging from 0n44 to 0n56 (Table 2) and were similar
when based on individual environments or across
environments. For DSI there was no obvious re-
lationship between stress of the environment and
magnitude of heritability estimates. Increased disease
at an environment did not always result in greater
heritability. The greatest heritability was obtained at
the Bulnes 1999 environment, which had the smallest
average DSI rating. The dierences in the reaction of
the F
$
derived-lines across all environments are
expressed by a signicant genotypeenvironment
interaction and consequently the smallest heritability
estimates, h# l0n44. Condence interval widths (here-
after width), which were consistent at each environ-
ment and across environments, ranged from 35 to
50% as large as the heritability point estimate. The
heritability of disease reaction was estimated more
precisely whenbasedonthree individual environments
(F
!
n
!&
:
##'
,
##(
l1n25; widthl49n82, 34n88 and 45n57%
respectively) than when based on data combined over
all environments (F
!
n
!&
:
##'
,
%&#
l1n21; widthl
50n30%).
In an attempt to determine the reliability of single
measures of DSI rating, the correlation between
50 x. :. bi rrNzo ET AL.
Table 1. Estimates of means and their standard errors for MRC disease severity index (DSI) rating in the parent
lines (BLS14 and Mo17) and 227 F
$
derived-lines measured at each individual environment and across
environments in RTo Cuarto
Environment*
Genotype SA99 BU99 SA00 Across environments
BLS14 12n73p0n04a 7n21p0n11a 11n11p0n02a
Mo17 53n33p0n35b 61n90p1n90b 55n55p0n23b
F
$
45n79p1n11b 29n35p0n99 64n42p1n03b 46n60p0n72b
LSD 39n11 32n35 35n65 25n82
* SA99 lSampacho (1999) ; BU99 lBulnes (1999) ; SA00 lSampacho (2000).
Column means followed by the same letter were not signicantly dierent at the 0n01 probability level, according to a t-
test.
Least signicant dierence for comparing the means of individual F
$
derived-lines at Pl0n05.
120
90
60
30
0
0 10 30 40 50 60 70 80 90 20 100
Disease severity index (DSI)
N
u
m
b
e
r

o
f

f
a
m
i
l
i
e
s
BLS14 Mo17
Fig. 1. Distribution of F
$
derived-lines for disease severity
index (DSI) in three environments. Parental mean values are
indicated.
measures on F
$
families in two environments were
calculated (Table 3). The simple correlations for DSI
rating of lines were not signicant between the means
of the SA00 and BU99 environments. Although the
correlations betweenthe SA99andSA00environments
and between the SA00 and BU99 environments were
signicant, these were too small to indicate that
families did not rank similarly in individual environ-
ments for MRC resistance, thus accounting for the
excess of genotypeenvironment interactions for this
trait.
The distribution of F
$
family means for plant
height, leaf surface, leaf border, leaf length and tassel
type in the separate environments and over all
environments followed approximately a normal dis-
tribution, with transgressive segregants noted in both
directions. Broad-sense heritability estimates for the
ve traits using variance components from F
$
family
means across three environments ranged from 0 to
0n48 (Table 4). Accuracy among estimates with 90%
condence limits varied widely as demonstrated by
dierences in the condence interval widths. Heri-
tability estimates and condence interval widths of
partial resistance to MRC based on individual
environments or across environments were similar to
that obtained for plant height (h# l0n48; widthl
42%) and tassel type (h# l0n38; widthl66%). The
various leaf traits expressed a very low heritability.
The computed heritability for both leaf surface and
leaf length were h# l0 and for the leaf border h# l
0n12. In addition, condence interval widths for the
leaf border, which was 225% as large as the
heritability point estimate, did not indicate a reliable
estimate of heritability.
On the basis of means of each F
$
derived-lines,
disease severity index signicantly (P0n01) corre-
lated with plant height, leaf surface, leaf border, leaf
length and tassel type (Table 3), with the correlations
being more pronounced at individual environments
with the most disease. Plant height correlated nega-
tively with DSI values in the SA99 and BU99 environ-
ments, in the SA00 environment and across the three
environments (r lk0n60, k0n55, k0n61 and k0n73
respectively). This signicant linear association be-
tween plant height and disease severity to MRCacross
environment showed that DSI rating dierences
among F
$
derived-lines could explain 53% of the
variation in plant height. Tassel type also correlated
with DSI rating at three individual environments (r l
0n54, 0n44 and 0n64) and across environment (r l
0n62). Signicant positive association for data com-
bined over all environments showed that 38% of the
variation in tassel type could be accounted for by DSI
dierences among F
$
families. Similar positive corre-
lations showed relationships among DSI rating with
leaf surface, leaf border and leaf length rating across
all environments and for individual environments.
Resistance to viral disease in maize 51
Table 2. Estimates of variance components, broad-sense heritability, and condence intervals (CI) for MRC
disease severity index (DSI) rating in 227 F
$
derived-lines measured at each individual environment and across
environments in RTo Cuarto
Environment*
Parameters SA99 BU99 SA00 Across environments
Variance components
#
g
173n58p39n23 172n74p31n79 158n62p33n90 78n04p8n25
#
e
390n43p36n73 269n50p25n52 325n89p30n66 90n56p0n18
#
ge
328n30p17n04
Heritability h# 0n47 0n56 0n49 0n44,
90% CI on h# 0n340n58 0n450n65 0n370n59 0n320n54
Width* 49n82 34n88 45n57 50n30
* SA99 lSampacho (1999) ; BU99 lBulnes (1999) ; SA00 lSampacho (2000).
With standard errors.

h# l(#
g
)\[(#
g
)j(#
e
\r)].
,
h# l(#
g
)\[#
g
)j(#
ge
\l)j(#
e
\lr)].
* Expressed as the ratio ( %) of the condence interval width relative to the heritability point estimate.
Table 3. Correlations of DSI rating for 227 F
$
derived-lines among three RTo Cuarto environments and phenotypic
correlations between DSI rating and agronomic traits
Environment
Environment* Agronomic traits
BU99 SA00 Plant height Leaf surface Leaf border Leaf length Tassel type
SA99 0n06 NS 0n19** k0n60** 0n27** 0n34** 0n42** 0n54**
BU99 0n19** k0n55** 0n12** 0n26** 0n32** 0n44**
SA00 k0n61** 0n41** 0n52** 0n40** 0n64**
Across environments k0n73** 0n38** 0n57** 0n44** 0n62**
* SA99 lSampacho (1999) ; BU99 lBulnes (1999) ; SA00 lSampacho (2000).
** Signicant at the 0n01 probability level ; NS, not signicant.
Table 4. Broad-sense heritability estimates with 90% condence limits for agronomic traits of 227 F
$
derived-lines
across environments in RTo Cuarto
Trait Heritability Low limit Upper limit Width*
Plant height 0n48 0n37 0n57 41n67
Leaf surface 0n00
Leaf border 0n12 0n00 0n27 225n00
Leaf length 0n00
Tassel type 0n38 0n24 0n49 65n79
* Expressed as the ratio (%) of the condence interval width relative to the heritability point estimate.
DISCUSSION
The primary cause for the abundance of disease in the
SA99 and SA00 environments was probably the result
of the sowing of the experimental trial in a lot of oat.
Oat appears to be one of the preferred hosts for the
vector (D. kuscheli) since the insects nd an optimum
environment to complete their development and then
migrate to adjacent maize crops. Considering this, the
SA99 and SA00 environments were the most severely
stressful and the BU99 environment appeared as the
least stressful.
The reaction to MRC disease, which is quan-
titatively inherited and probably controlled by a
polygenic system, showed transgressive segregation
suggesting the possibility of deriving resistant material
52 x. :. bi rrNzo ET AL.
from this segregating F
$
population. The absence of
dierences between the disease rating mean of the
susceptible parent Mo17 and the disease rating mean
of F
$
lines suggests partial recessiveness of resistance
for MRC disease indicating the presence of non-
additive gene eects (i.e. dominant and\or epistatic
gene action). These ndings are consistent with
previous reports about the quantitative inheritance of
MRC resistance (Presello 1993; Presello et al. 1995).
These authors found that additive and epistatic eects
were signicant. Because of the partial recessiveness,
which preclude any simple additive gene action model,
a portion of the genetic variance (#
g
) for reaction to
MRC is attributable to a non-additive component.
Epidemics of MRC are produced when there is a
combination of environmental conditions which lead
to abundant populations of migrant forms of D.
kuscheli, and when vectors spread during an early and
vulnerable growing stage of maize (Ornaghi et al.
1993). In a study with a segregating F
$
population
there is a wide range in plant development at the time
of inoculation and there is the risk of escape or limited
infections. The inconsistent responses of most families
across environments account for the substantial
genotypeenvironment interaction and the poor as-
sociation between DSI values in the dierent environ-
ments. These results indicate that evaluation of F
$
derived-lines for disease resistance to MRC requires
additional environments to obtain estimates of DSI
that are predictive of the performance of lines at other
environments and also explain why the breeding
eorts have been so laborious and time consuming.
The heritability estimates for partial resistance to
MRC showed consistent trends over the three
individual environments. Despite the signicant geno-
typeenvironment interaction, heritability estimates
are of a similar magnitude among the environments
and across environments. Accuracy among estimates
were similar as demonstrated by similarity in the
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was supported by grants from Agencia Nacional de
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Co! rdoba Ciencia and Universidad Nacional de R!o
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