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Introduction Fungal diseases are responsible for considerable yield losses in sugarcane crop. About 160 fungi have been reported to infect sugarcane, while seven diseases with unknown etiologies have been recognized and documented (Rott, 2000). Fungal diseases reduce cane yield by up to 31% (Jayashree et al., 2010). Among them, the most common disease is red rot, which is also known as a "cancer" of sugarcane (Khan et al., 2011), and is caused by the fungus Colletotrichum falcatum Went. Red rot severely affects the quantity and quality of the cane, with about a 29% reduction in cane weight and 30% less sugar recovery (Hussnain and Afghan, 2006). Red rot is one of the major, oldest, broadly distributed, and documented diseases of sugarcane in many countries, including Pakistan, the United States, Bangladesh, Taiwan, and Thailand (Viswanathan and Samiyappan, 2002; Viswanathan, 2012). It infects the sugar cane stalk at both the initial and mature stages of growth, causing discoloration, while the pathogen-produced invertase enzyme causes sucrose inversion in addition to drying of the cane stalks. Thus, overall, the vegetative growth of the plant halts (Sharma and Tamta, 2015). Various methods are adopted for red rot disease management, including chemical, biological, breeding, and tissue culture methods. All of these have certain limitations and disadvantages. For instance, chemical methods increase the cost of production and contaminate the environment as well, while biological control applied through plant growth-promoting bacteria (Malathi and Viswanathan, 2013) does not show consistent results in the field. Similarly, in tissue culture, the selection of fungus-resistant cells (Mohanraj et al., 2003; Sengar et al., 2009) is most often associated with somaclonal variations. Red rot-resistant varieties can be produced by breeding methods (Agnihotri, 1996), but breeding is laborious and time-consuming. To overcome all these limitations, genetic modification is the best available option for management of red rot disease in sugarcane crops. Specific genes can be introduced into the genome of sugarcane to create resistance against a particular pathogen (Enríquez-Obregón et al., 1998).

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The gene sequence encoding the mannose-binding homodimeric protein Allium sativum leaf agglutinin (ASAL) was introduced into maize inbred lines to achieve resistance against sap-sucking corn leaf aphids in transgenic lines. Maize transformants were generated after the co-cultivation of immature maize embryos with the Agrobacterium strain LB4404 harbouring a recombinant Ti-binary ASAL construct driven by the polyubiquitin promoter. The preliminary screening of maize transformants was performed via GUS histochemical analysis, and PCR and Southern blotting confirmed the insertion of the transgene and its stable integration in five transgenic maize lines. Transcript abundance was quantified by a quantitative real-time PCR assay, which revealed variable expression of the ASAL transgene among five transgenic maize lines. The highest mRNA expression of the ASAL gene was found in the A23 transgenic maize line, while the lowest expression was found in the AU1 transgenic maize line. In planta bioassays in the T 1 progeny of the transgenic maize lines revealed high resistance against corn leaf aphids compared to the control non-transgenic line. The mortality of the infesting aphids (Rhopalosiphum maidi) was found to vary from 40 to 71% compared to that of the non-transgenic control maize line. Keywords Corn leaf aphid . Mannose binding lectin . Transgenic maize . In planta bioassay Abbreviations ASAL Allium sativum leaf agglutinin GUS β-glucuronidase PCR Polymerase chain reaction TMVΩ TMVΩ translational enhancer T 1 first generation progeny plants Bt Bacillus thuringenesis NOS nopaline synthase gene * Bushra Tabassum

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Infection with enterotoxigenic Escherichia coli (ETEC) is a major contributor to diarrheal illness in children in low- and middle-income countries and travelers to these areas. There is an ongoing effort to develop vaccines against ETEC, and the most reliable immune correlate of protection against ETEC is considered to be the small intestinal secretory IgA response that targets ETEC-specific virulence factors. Since isolating IgA from small intestinal mucosa is technically and ethically challenging, requiring the use of invasive medical procedures, several other indirect methods are used as a proxy for gauging the small intestinal IgA responses. In this review, we summarize the literature reporting on anti-ETEC human IgA responses observed in blood, activated lymphocyte assayss, intestinal lavage/duodenal aspirates, and saliva from human volunteers being experimentally infected with ETEC. We describe the IgA response kinetics and responder ratios against classical and noncanonical ETEC antigens in the different sample types and discuss the implications that the results may have on vaccine development and testing.