Engineering resistance to L-phosphinothricin (glufosinate) in tobacco — which gene transfer has been used to confer resistance?

Introduction / Context:
Phosphinothricin (PPT, glufosinate) is a nonselective herbicide that inhibits glutamine synthetase (GS), leading to ammonia accumulation and plant death. Several strategies exist to engineer crop tolerance to this herbicide.

Given Data / Assumptions:

• Commercially, bar/pat genes (phosphinothricin acetyltransferase) are widely used, but they are not among the options.
• The biochemical target of PPT is GS.
• Altering or compensating for the target enzyme can impart tolerance.

Concept / Approach:

Because PPT inhibits GS, engineering plants with GS variants or overexpression can mitigate toxicity by maintaining glutamine synthesis. While EPSPS relates to glyphosate and ALS to sulfonylurea/imidazolinone herbicides, GS is the direct target of PPT and has been explored to enhance tolerance in research settings when bar/pat are not used.

Step-by-Step Solution:

Verification / Alternative check:

Although bar/pat are the dominant commercial solution, literature shows that modifying GS expression or insensitivity can contribute to tolerance in experimental systems.

Why Other Options Are Wrong:

EPSPS and ALS confer tolerance to different herbicide classes; “Any of the above” is incorrect because only GS directly aligns with PPT’s target among the listed genes.

Common Pitfalls:

Assuming all herbicide resistance relies on the same target modifications; each herbicide class has specific targets.

Final Answer:

Gene for GS (glutamine synthetase)