I sometimes use 2,4-Dichlorophenoxyacetic acid to control broadleaved weeds in lawns. It is selective, and quickly kills the dicot weeds, while other plants are unharmed.
2,4-D is a synthetic auxin, a class of plant hormones. It is gets taken in through the stomata on the leaves, and is transported to the meristems of the plant. This causes uncontrolled, unsustainable growth, and the plant wilts, and dies.
Why doesn't this affect most monocotyledons?
According to this link from Purdue, the seed of the answer is this:
The herbicide is used to kill broadleaf weeds, which are dicots, while monocot grasses, such as sorghum and corn, are more resistant. That's because grasses inactivate 2,4-D inside the plant, while broadleaf dicots do not.
But on the other hand, Song 2014 has this to say about 2,4-D:
However, the underlying molecular mechanism of how auxinic herbicides selectively kill dicots and spare monocots is not understood yet (Grossmann 2000; Kelley and Riechers 2007; McSteen 2010). The mechanisms of auxin biosynthesis, transport, and signal transduction are conserved in monocots and dicots make this question more complex (McSteen 2010). Early research has proposed that the selectivity of auxinic herbicide is because of either limited translocation or rapid degradation of exogenous auxin, altered vascular anatomy, or altered perception of auxin in monocots (Monaco et al. 2002; Kelley and Riechers 2007). Auxin transport is influenced by plant vascular systems (Mattsson et al. 1999; Scarpella et al. 2006). The difference in vascular tissue structure between dicots and monocots may contribute to the selectivity of auxinic herbicides. In monocot stems, the vascular tissues (the phloem and xylem) are scattered in bundles, and lack a vascular cambium; in dicot stems, the vascular tissues are form ed in rings and possess a cambium.
So in other words, we don't know yet. It seems to be very strongly tied to auxin transport, but we do not have the full mechanism of action; since auxin is such an important plant hormone, and the pathway is therefore highly conserved (that is, the genes tend to be nearly identical on the parts of the sequence that affect the phenotype), the general conclusion is that the pathway itself is not affected, but an accessory pathway clears up auxin in levels excess of any normal amount in monocots.
Edit: Whoops, got the author's first/last names mixed up.
The specificity of 2,4 D may be due to either limited translocation or rapid degradation ,altered vascular anatomy or altered perception of auxin in monocot
