Plastidic MSH1 Suppression for Plant Trait Breeding
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Solution Overview
Problem
Current methods for introducing heritable and epigenetic/genetic variation in plants to exhibit useful traits, such as nuclear and maternal inheritance, are limited in their ability to prevent mitochondrial recombination and effectively utilize plastidic MSH1 suppression in conjunction with mitochondrial-targeted MSH1.
Innovation Solution
The method involves crossing plants with suppressed plastidic MSH1 in the presence of mitochondrial-targeted MSH1, followed by selection of progeny plants with recovered MSH1 function to produce plants exhibiting desired traits, including nuclear and maternal inheritance, while avoiding undesirable phenotypes like mitochondrial recombination.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Productivity
If plastidic MSH1 is suppressed to induce heritable epigenetic variation and useful traits, then plant breeding outcomes are improved, but mitochondrial recombination occurs as an undesirable side effect
Solution Approach 1:
The patent uses a conditional promoter system as an intermediary mechanism that allows selective suppression of plastidic MSH1 only under specific conditions (presence of tetracycline or its derivatives). This mediator approach enables researchers to induce desired epigenetic variation while controlling the timing and extent of MSH1 suppression, thereby reducing unwanted mitochondrial recombination events.
Solution Approach 2:
The patent employs parameter changes by utilizing different antibiotic agents (tetracycline, doxycycline, oxytetracycline) and their concentrations to modulate the level of MSH1 suppression. By adjusting these chemical parameters, the system can achieve optimal suppression levels that induce useful epigenetic traits while minimizing harmful mitochondrial recombination.
2Quantity of substance
If MSH1 suppression is applied to both plastids and mitochondria, then epigenetic variation is induced, but mitochondrial recombination increases significantly
Solution Approach 1:
The patent segments the MSH1 gene function by creating tissue-specific and organelle-specific suppression. The conditional promoter system allows MSH1 suppression to be restricted to plastids only, while mitochondrial MSH1 remains functional. This segmentation prevents the harmful interaction that would occur if both plastidic and mitochondrial MSH1 were simultaneously suppressed.
Solution Approach 2:
Instead of suppressing MSH1 in both plastids and mitochondria simultaneously, the patent inverts the approach by selectively preserving mitochondrial MSH1 function while suppressing only plastidic MSH1. This inversion strategy maintains mitochondrial stability while still achieving the desired epigenetic variation in the nucleus.
3Stability of the object's composition
If recurrent selection is used to establish stable epigenetic states, then heritable traits are achieved, but the process requires multiple generations increasing time investment
Solution Approach 1:
The patent applies preliminary action by using the conditional MSH1 suppression system to pre-establish epigenetic modifications in controlled conditions before formal breeding programs. The conditional promoter allows researchers to induce and stabilize desired epigenetic states in advance, creating pre-conditioned plant lines that require fewer generations of recurrent selection to achieve stable heritable traits.
Data Source
AI summary
The present disclosure provides methods for obtaining plants that exhibit useful traits or that are useful for plant breeding by suppression of plastidic MSH1 in the presence of mitochondrial-targeted MSH1 in plants. Methods for identifying genetic loci that provide for useful traits in plants and plants produced with those loci are also provided. In addition, plants that exhibit the useful traits, parts of the plants including seeds, and products of the plants are provided as well as methods of using the plants. Recombinant DNA vectors and transgenic plants comprising those vectors that provide for suppression of plastidic MSH1 in the presence of mitochondrial-targeted MSH1 are also provided.