Cotton (Gossypium hirsutum L.) is greatest central cash crop of Pakistan which belongs to Gossypium Genus and Malvaceae family (Brubaker et al., 1999a).Cotton consist more than 50 species together with wild as well as cultivated. (Fryxell, 1979) reported that there 45 species are diploid and five are allotetraploid in nature. The status of cotton is obivious from circumstance that it is not one of most important fiber crop rather it is also second most important oilseed crop of the world (Cherry and Loffler, 1984). (Riaz et al. 2013) reported that cotton is grown in warmer climates in overall world. Pakistan has made substantially increase 11.2 times lint production and 4.4 times seed cotton yield per acre since 1947 but still there is wide gap of cotton yield between our and other advanced cotton growing counties in overall world (Ahmad, S., et al 2010).The environmental changes including biotic and abiotic stresses are major threats to food security and agricultural production. Biotic stresses including viral diseases are responsible for huge losses in production and quality in all parts of the world as well as in Pakistan. Cotton leaf curl virus (CLCuV) is furthermost damaging disease which results a huge losses (Khan and Ahmad, 2005). Cotton leaf curl virus is most important causes establishing primary limit (Watkins, 1981; Briddon et al., 2000).This mini review will help to obtain information about cotton leaf curl viral disease and their control through conventional and biotechnological tools.
Background of CLCuV
Farquarson,(1912) studied that in 1912 cotton leaf curl virus was first time reported on Gossypium barbadense in Nigeria. This disease was occurred suddenly with minor problem including second time epidemic occurring in 1924 in Nigeria. After 1912, it was recorded in 1924 in Sudan where it was found to be transmitted under natural condition through grafting and whitefly (Bailey, 1934; Jones and Mason; 1926). Jones and Mason, (1926) reported that this disease became a major component in the reducing long stable cotton production until before 1960 in Gezira and Tanzania. In 1926, CLCuDwas reported in Tanzania and in 1959, it was found in Philippine (Hussain and Ali, 1975). In 1993, this disease was first time reported in India on G.hirsutum in Spriganagar area which is present in Rajasthan state (Ajmera, 1994). (Rishi and Chauhan, 1994; Singh et al, 1994) studied that CLCuV was appeared in 1994 in Haryana and Punjab states on American upland cotton and it introduced a major threat to cultivation of cotton in Northern India (Verma et al., 1995). Cotton leaf curl virus is one of the major factor which results a primary limit in cotton production (Watkins, 1981; Briddon et al., 2000). In the Pakistan, this disease was first time found on few individual plants of Gossypium hirsutum L. at Khokhran which is near the Multan (Hussain & Ali, 1975). This disease was not such a serious problem in the beginning but with passage of time it became an alarming and potential threat to many of cultivars of cotton (Hussain and Ali, 1975). After 1991-92, it became a serious and alarming threat for cotton production with continuousness till in 1996 with the development of resistant variety of cotton against CLCuV (Ahmad, S et al., 2010). Mansoor et al., (2003) reported that during 2001 in Burewala this disease arose again breaking resistance which was present in all available lines of cotton. Now this became a destructive disease of cotton in Punjab area of Pakistan. Due to almost same symptoms of Burewala virus to previous CLCuV, this virus is only 8% different from previous virus which was examined on molecular basis (Mansoor et al., 2003).
Symptoms of plants which are infected by cotton leaf curl disease may be vary, it depends on the disease severity (Farooq, A et al., 2011). Farooq, A et al., (2011) reported that symptoms of this disease typically are yellowing and thickening of smaller veins that are present on the lower surface of younger leaves. There are two kinds of vein thickening of CLCuV are seen, first small vein thickening and second main vein thickening (Ahmad, S et al., 2010). (Mansoor et al., 1993; Nateshan et al., 1996) reported that initial symptoms of CLCuV contained of temporary vein clearing on young leaves. Leaves curl upward or downward with plant growth which are stunted under severe attack of disease due to reduction of distance between nodes (Briddon et al., 2001; Qazi et al., 2007). During severity of this disease, infected leaves also produce a cup shape outgrowth on the lower side of curled leaves that is named as Enation (Mansoor et al., 1993; Harrison et al., 1997). (Rehman et al., 2000; Monga et al., 2011) reported that at the seedling stage, appearance of this disease was such serious that retards flowering, boll formation, maturation, fiber quality and seed cotton yield.
There are different climatic factors which are involved in development of cotton leaf curl virus disease (CLCuD) such as temperature, wind and rainfall in Africa (Farooq, Amjad, et al.2011). Blink, (1975) reported that seedling before rainfall may be posed an increased population of vector due to abundance supply of food source. Ahmed et al, .2013 reported there are significant correlation between temperature and CLCuD and between PAN evaporation and CLCV during month of July in Multan district of Pakistan which is regarded to be the hot spot area for the development of this disease. (Farooq, J., et al,.2014) reported that cotton which is grown only for part of year, cultivated host and alternate weeds function as reservoirs for virus.
Primary sites of infections and fields in which cotton is infected by whitefly are established (Farooq, J., et al,.2014). Primary sites of infections and additional vectors serve as secondary spread of this disease to other plants which during whole growing season enter in the field (Giha and Nour, 1969). Khan et al. (1998) studied by using regression analysis on air temperature ( maximum and minimum ) ,relative humidity, wind movement and rainfall association with percentage of plants which are infected by Cotton leaf curl disease on eighty cotton varieties. Rate of infestation of disease increased in range of minimum and maximum temperatures of 25-30oC and 33-45oC respectively (Khan et al. (1998). They also studied that a non-significant correlation between intensity of CLCuD and population of whitefly and poor correlation of humidity and weekly rainfall with development of disease (Khan et al. (1998). Akhtar et al., 2002b reported that there is non-significant correlation of % relative humidity (5p.m.), wind velocity, sunshine, maximum weekly air temperature (oC) and population of whitefly on thirteen varieties. They reported that there is a negative correlation for development of CLCuV disease between velocity of wind (8 a. m.) and minimum temperature of air (Akhtar et al., 2002b. They also found positive correlation that exist between plant age and percentage of disease incidence (Akhtar et al., 2002b). Maximum percentage of disease index that was recorded at 6 week old seedlings is gradually decreased with increase in age of plant (Farooq, J., et al,.2014). (Briddon et al., 1998) reported many researchers observed non-significant relationship that is present between CLCuD and population of whitefly.
Genetic Bases or Inheritance of Resistance to Cotton leaf curl virus (CLCuD)
Tarr (1951) studied that resistance that is expressed to cotton leaf curl disease is an unstable character. According to study of Knight (1948) CLCuD is controlled through a major gene. There are two dominant genes that control development of cotton leaf curl virus disease in upland cotton (Randhawa, 1999). (Hutchinson and Knight, 1950) reported that breeding for development of resistance against cotton leaf curl disease has been acquired through involvement of assemblage of minor genes by using recurrent selection. Resistance which depends on major genes (dominant genes) against CLCuD may be no longer remains and lost quickly because of evolution of pathogen that is occurred for these genes (Azhar et al., 2010). According to study of Ali (1999), Rehman et al. (2002) and Haider (2002), it was suggested that CLCuD is under control of single gene having dominant effects. Two dominant genes control CLCuD that behaved as dominant epistasis in controlling resistance against CLCuD (Iqbal et al., 2003). There are three genes that involved in resistance to CLCuD in upland cotton (G.hirsutum) (Rehman et al., 2005). They reported that out of three genes, two genes function as resistance to CLCuD (R1 CLCuD hir and R2 CLCuD hir) and third gene that is suppressor gene that serves as to suppress resistance (sCLCuD hir) (Rehman et al., 2005). While Ahuja et al., (2006) reported that there are two genes involved in resistance to CLCuD with duplicate dominant, dominant inhibitory and duplicate recessive non-allelic interaction (epistasis) and three genes with triplicate dominant epistasis. Khan et al.,( 2007) reported that inheritance of resistance for CLCuD is not known, it is still under discussion whether it is nuclear ( nucleus) or extra-nuclear (cytoplasm) but both reports that maternal effects are present. Khan et al., (2007) reported quantitative inheritance for resistance against CLCuD with predominance of additive gene effects. But according earlier the findings, it was observed that a major gene functions in controlling resistance of CLCuD along with another minor gene (modifier genes) Siddiq, (1970). Since resistance source against CLCuBuV (Cotton leaf curl burewala virus) is not present in American upland cotton but through gene pyramiding, genetic tolerance can be intensified (Iqbal,M et al., 2014). There are two new cotton genotypes IUB222 and MNH 886 have developed against this disease by gene pyramiding which are highly tolerance to this disease (Anonymous, 2011b). According to Aslam et al. (2000), a cross which is made between Gossiupium barbadense L. (Giza-45) and Gossiupium hirsutum L. (Reba P-288) determined the presence of effect of a single dominant gene. The F1 of crosses which is made between highly susceptible S-12 and highly resistant LRA-5166 varieties were all plants free from virus and their F2 was found close to 1:3 ratio which indicate presence of single gene which has inheritance of resistance for CLCuD( Mehmood (2004) and Rehman et al. (2005). While in the same cross (LRA-5166 x S-12), there is no single gene with major effect that responsible for cotton leaf curl disease reported by (Khan et al., 2007).
Screening methods for CLCuD
There are many screening methods which are used for cotton leaf curl disease. The most common screening methods which are used in the field are described below.
Sick Plot Technique
It is any easy method that is used for the phenotypic evaluation of the target varieties and is practiced commonly at variously Cotton research station (CRS) (Iqbal, M et al., 2014). A susceptible genotype S-12 is used in this technique (Anonymous, 2013), this susceptible genotype functions as spreader in rows between the genotypes to be tested keep in 1:3 ratios (Shah et al., 2004; Perveen et al., 2005).
Many scientists used this method scientist (Ali M. 1997; Akhtar et al., 2004; Shah et al., 2004 and Mansoor et al., 2003a). In this method the root stock of cotton genotype which is used to be tested against CLCuD and scion contained of the susceptible source of disease inoculums that is used to transmit the disease in stock plants ,later on presence of virus is confirmed visually and then by ELISA test (Farooq et al., 2011). Bottle graft, top cleft and wedge graft are three procedure of grafting that are mostly used by the researchers practically.
New genotypes of cotton or segregating population in F2 are screened against cotton leaf curl disease by normal and late sowing including with the disease nursery (Khan et al., 2000; Ahuja et al., 2006; Perveen et al., 2010; Iqbal et al., 2011).
The occurrence of CLCuD reached maximum within 40-50 days after sowing in late sown cotton (first week of July) while in early sowing ( second and third week of April ) attack of the CLCuD occurs almost 100 days after sowing(Iqbal et al.,2010).Therefore, screening of candidate genotypes or segregating material for tolerance against infestation of CLCuD should be panted in the 1st or 2nd week of July so this method is economically most feasible to screen germplasm, segregating population and candidate varieties against CLCuD tolerance.
Mahmood et al.(1994); Monga et al. (2011) reported this method of screening of cotton germplasm against cotton leaf curl disease is very useful in which cotton germplasm is screened by using viruliferous whiteflies that used as an inoculation source in net cages on test plants.
Control measures (Non-Biotechnological tool) and Recommendations
The development of tolerant varieties against disease is one of the solution still but when resistance sources become inadequate then management of disease is quite appropriate (Farooq, A et al., 2011).In cotton, host plant resistance is long term and explored strategy that is used to protect plants from attack of CLCuD (Jones, 2001; Solomon-Blackburn and Bradshaw, 2007).
Monga et al., (2001) reported the primary inoculum that exist in the form of weeds during off season and other hosts is major source to spread cotton leaf curl disease.The control of vector whitefly and eradiation of weeds that contribute the hospitality of cotton leaf curl virus are strategies that are used for management of CLCuD (Narula et al., 1999; Monga et al., 2001).
The plants escape from the most susceptible stage by using insecticides even if infection occurs at later stage and severity of losses may be avoided when symptom will begin to appear after 65-90 days (Singh et al., 2002; Monga et al., 2011).
Numerous agronomic practices such as sowing time and application of nutrients (Nitrogen and Potassium) can cause severe disease problem as choosing best sowing time for specific variety in different region is difficult so too early and too late sowing may cause problem of disease and pests(Farooq, A et al., 2011).
Ghazanfar et al., (2007) reported suitable time of sowing preferably mid April to mid May results in decrease in occurrence of disease as compared to late sowing form mid May to June.
If distance between plant to plant is increased in the case of early sowing and decreased under late sowing condition than it is effective in management of cotton leaf curl disease ( Iqbal M, Khan MA ,2010).They also determined that infestation of CLCuD reached it maximum after 105 days of sowing while in case of late sown crop i.e. 15 June or late infestation becomes severe after 45 days of sowing so they suggested 15 cm plant spacing that is appropriate to manage CLCuD in the case of planting later than 15 th of June.
The appropriate concentration of Nitrogen in the case of susceptible cultivars plays a vital role to tackle severity of disease while this Nitrogen concentration does not effect on resistant cultivar (Farooq, A et al., 2011).Zafar et al., (2010) reported that the strategies can be planned to prevent, escape, avoid and control viral disease by understanding physiological basis of nutrition (Nitrogen).
The virus resistant cultivars, management of causative agents and mineral nutrition are most recommended management practices that are used to handle CLCuD disease (Akhtar et al., 2004). Kafkafi et al., (2001) reported effect of Potassium (K) application on disease through specific metabolic functions change relationship of host-parasite environment.
According to experiment of Pervez et al., (2007) that was conducted on role of Potassium in the control of cotton leaf curl disease, it was concluded that improved application of Potassium (K) up to 250 kg/ha results in the reduction of disease which is about from 12 to 38%.This increased application of potassium added considerably as seed cotton yield increased which is increased up to 37% as compared to zero-K.
Recent advances to combat CLCuV through biotechnological tools
Due to abrupt changes in climatic condition and accessibility of limited resources, conventional breeding methods is not successful and have certain limitations, so now it is easy to combat cotton leaf curl virus (CLCuV) by cloning certain virus due to advancement in biotechnological methods and develop controlling strategies(Farooq et al., 2011).
Agrios (1997) reported during domestication of plants from wild to cultivated forms, diseases have caused a hug loss in yield.
The main problem that plant breeder has to face is the introgression of resistance traits controlling genes for development of resistance in plants through using conventional procedure of breeding (Farooq et al., 2011). Now a days, the crop plants may have resistance against certain disease that is developed by genetic engineering and this resistance against certain pathogens is controlled by single or multiple genes (Crute and Pink, 1996).
Pathogen disease resistance (PDR) methodology by RNA mediated technology (sense and anti-sense RNA mediated) and protein mediated resistance has been recognized to combat different viruses due to lacking of natural resistance against diseases in plants.Many genes have been integrated in a number of plants which are used to engineer PDR especially in those crops in which natural resistance genes are not found (Gallitelli and Accotto, 2001).
American upland cotton (Gossipium hirsutum L.) is free from CLCuD and various other viral and fungal diseases (Briddon and Markham, 2001).Through genetic transformation approach, resistant genes are isolated and incorporated into susceptible varieties (Farooq 2011).
Molecular markers that are related with cotton leaf curl virus disease resistance can improve the efficiency of selection in the breeding programmes (Farooq 2011).