For more than two decades, the evolution of glyphosate resistance was not perceived as a problem (Bradshaw et al., 1997). This opinion was based on the difficulty of discovering a fully functional EPSP synthase that was insensitive to glyphosate; the inability of plant species to enzymatically deactivate glyphosate; the lack of soil activity of glyphosate (thus reducing the selection pressure due to exposure); and the empirical observation that no resistant weeds had appeared after at least 20 years of usage.

The three most likely ways for weeds to develop resistance to glyphosate did not seem likely (Jasieniuk, 1995). Over-production of the EPSP synthase target site did not increase resistance enough for plants to survive glyphosate amounts used in agricultural settings (Kishore and Shah, 1988). The EPSPS modifications that conferred glyphosate resistance in bacteria were inside the enzyme’s active site, which reduced its catalytic efficiency and thus would probably reduce plant fitness (Padgette et al., 1995). No higher plants could be found with even low levels of ability to metabolically inactivate glyphosate (Dyer, 1994).

However, the views about the capacity of weeds to develop glyphosate resistance changed in 1996 when a glyphosate-resistant weed, Lolium rigidum, was discovered in Australia (Pratley et al., 1999; Powles et al., 1998). Since then, glyphosate resistant biotypes in at least 10 other weed species have been confirmed (Nandula et al., 2005), and more than a million hectares are now infested with resistant weeds. Some of these biotypes exhibit resistance at application rates 4 to 13 times higher than susceptible populations.

The most widespread glyphosate-resistant weed is marestail (Conyza canadensis). Glyphosate resistant marestail was confirmed in 2000 (VanGessel, 2001). Marestail produces very large numbers of light, wind dispersed seed and can cross-pollinate, leading to widespread infestation of no-tillage crop and non-crop land. As a result, five years after its first occurrence, it was found on a half-million hectares across the U.S. Midwest, South and Atlantic states (VanGessel, 2001; Heap, 2005). Dose response analysis showed these populations were eight to 13-fold more resistant that susceptible marestail populations.

In 2002 and 2003, farmers, consultants and extension agronomists frequently observed common lambsquarters (Chenopodium album), a significant problem in row crops, as the only surviving weed in soybean fields after glyphosate usage. Farmers and extension agents thought factors other than endogenous resistance, such as an inability of glyphosate to penetrate lambsquarters thick cuticle, might explain persistence after glyphosate expsoure. However, King et al (2004) recently confirmed some common lambsquarters biotypes in Virginia are glyphosate resistant.

Significant populations of common and tall waterhemp (Amarathus sp.) that survived glyphosate application were first observed in fields in Iowa, Illinois, and Missouri (Owen, 2002; Smeda and Schuster, 2002). Studies indicate that plants survived glyphosate rates 2.6 times the label rate and some waterhemp plants have now been classified as glyphosate resistant (Owen and Zelaya, 2005).

The molecular basis for weed resistance to glyphosate is not understood in most cases.  Initial studies of various weed species revealed EPSPS target site insensitivity (Braerson et al., 2002). Differences in translocation and transport to the chloroplast are also important in some weeds (Lorraine-Colwill et al., 2003; Feng et al., 2004). The mechanisms of glyphosate resistance in other weeds appear to be complex and polygenic.