Inheritance of Wheat Streak Mosaic Virus Resistance in KS03HW12

Research Article

Austin J Plant Biol. 2015;1(1): 1001.

Inheritance of Wheat Streak Mosaic Virus Resistance in KS03HW12

Zhang G*, Seifers DL and Martin TJ

Agricultural Research Center-Hays, Kansas State University, USA

*Corresponding author: Zhang G, Agricultural Research Center-Hays, Kansas State University, Hays, KS 67601, USA

Received: May 22, 2014; Accepted: June 15, 2014; Published: June 19, 2014


Wheat streak mosaic caused by Wheat Streak Mosaic Virus (WSMV) is a serious disease in wheat (Triticum aestivum L.). Use of cultivars with the WSMV resistance is a primary and effective way to control this disease. 'KS03HW12' is a newly discovered wheat line with the WSMV resistance. This study was conducted to determine the inheritance of WSMV resistance in KS03HW12 and its allelic relationship with a known resistance gene Wsm2. KS03HW12 was crossed to a susceptible line 'KS04HW87' and a resistant cultivar 'RonL' having the Wsm2 to obtain F1 and F2. Seedlings of parents, susceptible check, F1 and F2 were artificially inoculated and evaluated for WSMV reaction at 18oC in a growth chamber. A total of 144 F2:3 family lines from the cross of KS03HW12 x KS04HW87 were further evaluated for WSMV reaction. Data from the cross of KS03HW12 x KS04HW87 indicated a two-gene with recessive epistasis model for the WSMV resistance in KS03HW12. The F2 segregation ratio in the cross of KS03HW12 x RonL suggested there are different resistance genes between KS03HW12 and RonL. Therefore, resistance genes in KS03HW12 and RonL could be stacked to produce durable resistance.

Keywords: Wheat; Wheat streak mosaic virus; Inheritance; Epistasis; Allelism


WSMV: Wheat Streak Mosaic Virus; WCM: Wheat Curl Mite


Wheat Streak Mosaic Virus (WSMV: Tritimovirus, Potyviridae), transmitted by Wheat Curl Mite (WCM: Aceria tosichella Kiefer), is a destructive virus in wheat (Triticum aestivum L.). The WSMV causes sporadic epidemic in many regions around the world including USA, Canada, Europe, Russia, and Australia [1,2]. In the USA, WSMV has become common in the Great Plains [1]. The WSMV infected plants typically show symptoms such as yellow streaked leaves, stunted growth, reduced tillering, partially filled heads, and eventually considerable yield and quality reduction. The yield losses caused by naturally infected WSMV in Kansas have been reported as high as 13% with an average of 2% annually [3]. A WSMV epidemics occurred in Alberta in 1964 resulted in a yield reduction of 18% [4]. In artificially inoculated trials, Rahman et al. [5] reported a range of 21 to 70% in yield reduction due to WSMV infection among 38 winter/ spring wheat varieties while Sharp et al. [1] showed yield losses of 41 to 74% among nine locally adapted cultivars.

There are no effective chemicals available for controlling WSMV and its vector. Host resistance is a primary and effective way to control the WSMV disease in wheat. Using wheat cultivars with vector resistance is one possible method to reduce the yield loss caused by the WSMV [6-8]. However, the ability of WCM to quickly evolve from avirulence to virulence on a resistant cultivars makes this approach less cost effective [9-11]. An alternative way to control this disease is to enhance the host resistance to the virus itself. Since WSMV was first reported in 1920s [12], great efforts have been made to find resistance sources. High level of WSMV resistance was first identified in a wild relative, Thinopyrum intermedium (Host) Bark worth and Dewey [Agropyron intermedium (Host) P. Beauv.] [13- 16]. the resistance gene from Thin.intermedium, designated as Wsm1, has been introduced into cultivated wheat through translocation [17] and it has showed its effectiveness in reducing yield loss against the WSMV inoculation under field conditions [1]. However, yield penalty was observed from 11 to 28% among lines introgressed with Wsm1, indicating a linkage drag from the alien translocation [1]. Most recently, another resistance gene Wsm3 from Th. Intermedium was identified and translocated into conventional wheat [18]. Additionally, Fahim et al. [2] also discovered WSMV resistance in another wild species Th. scripeum. The WSMV resistance sources in cultivated wheat were found much later than the ones in wild species. Breeding line 'CO960293-2' was the first conventional wheat line with the WSMV resistance found in the USA [19]. Later on, two more resistant breeding lines, 'KS03HW12' [20] and 'CO960333' [21], were identified. Additional conventional wheat germplasm with the WSMV resistance has also been reported [2,19,22].

All the WSMV resistance sources found so far are temperature sensitive. Most resistance sources in the conventional wheat, including CO960293-2 and KS03HW12, can resist WSMV infections at 18°C and permit a systemic infection when exposed to a higher temperature for a certain period of time [18-20]. The resistance of Wsm1 and Wsm3 from the wild species can tolerate a higher temperature at 20°C and 24°C, respectively [16,20]. Field tests have showed that the WSMV resistance at 18°C in CO960293-2 and KS03HW12 were effective in protecting against yield losses caused by WSMV inoculation [18,23]. The WSMV resistance in CO960293-2 is reportedly controlled by a single dominant gene, which has been mapped to chromosome 3B and designated as Wsm2 [24]. CO960293-2 has been widely utilized in breeding programs and its WSMV resistance has been introgressed into two cultivars 'RonL' (PI 648020) and 'Snowmass' (PI 658597) [25]. However, with the deployment of WSMV-resistant cultivars, the limited resistance sources in these cultivars might be broken down by the selection pressure on the virus. Therefore, it is important to discover new resistance genes, which can be stacked with the existing resistance genes to make the resistance more durable.

The WSMV resistance source KS03HW12 was developed by the Agricultural Research Center-Hays at the Kansas State University and it was derived from a three-way cross of 'KS97HW29'/'KS97H W131'//'KS96HW100-5' [23]. If KS03HW12 processes resistance gene(s) other than Wsm1 and Wsm2, it could be a valuable and additional resistance source for breeding programs. It has been known that KS03HW12 did not have the Wsm1 based on the molecular marker analysis [23]. KS03HW12 has similar WSMV resistance as CO960293-2, but they do not share any common ancestors in their pedigrees according to our records. Therefore, it might be possible that KS03HW12 has a different resistance gene than Wsm2. However, the allelic relationship between the resistance gene(s) in KS03HW12 and Wsm2 has not been explored yet. It is very critical for us to define their allelic relationship in order to decide whether it is useful to pyramid these two resistance resources in breeding programs. Additionally, little is known about the genetic basis of the WSMV resistance in KS03HW12, which could hinder its utilization. By knowing its genetic control, breeding programs could choose appropriate methods to incorporate this resistance into superior cultivars more efficiently. Therefore, the objective of this project was to determine: (i) the inheritance of the WSMV resistance in KS03HW12; and (ii) the allelic relationship between the resistance gene(s) in KS03HW12 and Wsm2.

Materials and Methods

KS03HW12 was crossed with 'RonL' and 'KS04HW87' to obtain F1. KS04HW87 is a WSMV-susceptible wheat breeding line and it was developed by the Agricultural Research Center-Hays at the Kansas State University. Some F1 was selfed to obtain F2. F2 together with parental lines, susceptible check ('T81'), or F1 were seeded in 30 x 50 cm metal flats filled with potting mix for the WSMV evaluation. Each flat had 22 rows and 12 seeds were planted in each row. Parental lines, susceptible check, and F1 each were seeded in one row. The evaluation trial for the cross of KS03HW12 x KS04HW87 was conducted two times. In each trial, parental lines were planted in two replications. Due to limited number of seeds, F1 was only planted in the first trial. After evaluation in the first trial, F2 plants were vernalized and then transplanted into pots for generation advancement. A total of 144 F2:3family lines were obtained and they were seeded together with T81 and three replications of parental lines in flats for a WSMV confirmation test. Each F2:3 family line or parental line was seeded in one row. For the cross of KS03HW12 xRonL, parental lines, T81, and F2 were seeded in one flat. Plants in the flats were grown in growth chambers (Percival Model PGC-15WC) under 12 h photoperiod at 18°C.Plants at the single leaf stage were mechanically inoculated with Sidney 81 isolate as described by Seifers et al. [20]. The inoculated plants were rated for symptoms three weeks after inoculation on a scale of 1 to 5 (1: no visual symptoms, 2: a few chlorotic streaks, 3: moderate mosaic, 4: severe mosaic, 5: severe mosaic, necrosis, and yellowing). The segregation ratio of WSMV rating in the F2 populations was tested by chi-square for goodness of fit. The trials for the cross of KS03HW12 x KS04HW87 were used to determine the inheritance of the WSMV resistance in KS03HW12; and the trial for the cross of KS03HW12 x RonL was used to determine the allelic relationship between the resistance gene(s) in KS03HW12 and Wsm2.


The WSM rating for the cross of KS03HW12 x KS04HW87 is presented in Table 1. In the first evaluation trial, all 11 plants of susceptible check T81 was rated as 3 while the rating score for susceptible parentKS04HW87 was similar as T81 with 3 for all 10 plants in its first replication and 2 for two plants and 3 for eight other plants in its second replication. Both replications of KS03HW12 had no symptoms (rated as 1). Only two F1 plants were available and they had no symptoms as KS03HW12, indicating that WSMV resistance in KS03HW12 is dominant. The F2 plants were scored in a range of 1 to 3. The observed ratio among these three rating scores (1:2:3) fitted a 9:3:4 ratio (P=0.208), suggesting two genes with recessive epistasis conditioning the WSMV resistance in KS03HW12. To confirm the segregation ratio, this F2 population was seeded, inoculated, and evaluated for a second time. In the second evaluation trial, all plants of susceptible check T81 and susceptible parent KS04HW87 were rated as 3 while all plants of KS03HW12 were rated as 1. The observed segregation ratio (1:2:3) in the F2 population still fitted that 9:3:4 ratio (P=0.053). If combining these two sets of data, the segregation ratio fitted the 9:3:4 ratios very well with a probability of 0.629. Therefore, the result from the second evaluation trial further supported a two-gene with recessive epistasis model for the WSMV resistance in KS03HW12.