LRR-RLK Meristem Control for Higher Kernel Row Number
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Solution Overview
Problem
Existing methods for modulating meristem size in plants, particularly in maize, are inadequate for enhancing kernel row number and yield, often leading to aberrant growth and disorganized meristems due to uncontrollable expansion.
Innovation Solution
Introduce mutations in the Leucine Rich Repeat Receptor Like Protein Kinase (LRR-RLK) gene using CRISPR-Cas editing systems to create null, dominant negative, semi-dominant, or weak loss-of-function alleles, thereby controlling meristem size and increasing kernel row number without significantly reducing ear length.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Productivity
If meristem size is increased to initiate more flowers and increase kernel row number, then yield is improved, but the meristem becomes disorganized and aberrant growth occurs
Solution Approach 1:
The patent applies parameter changes by modifying the kinetic parameters of the CLV1 receptor through dominant-negative mutations. These mutations alter the phosphorylation activity and signaling threshold of the receptor, changing the dynamic range of meristem size control without disrupting the overall organizational stability of the meristem.
Solution Approach 2:
The invention utilizes dynamics by creating a tunable signaling system where the dominant-negative CLV1 receptors provide graded inhibition of WUS expression. This dynamic control allows the meristem to expand to an optimal size for increased flower initiation while maintaining self-regulation mechanisms that prevent disorganized growth.
2Productivity
If dominant-negative CLV1 alleles are used to expand meristem size, then flower number increases, but uncontrollable meristem expansion and fasciation occur
Solution Approach 1:
The patent implements feedback control through dominant-negative CLV1 receptors that continuously monitor and regulate WUS expression levels. The mutated receptors provide feedback inhibition that prevents WUS from exceeding threshold levels, thereby controlling meristem size and preventing fasciation while still allowing expansion beyond wild-type limits.
Solution Approach 2:
The invention applies partial action by using dominant-negative mutations that provide intermediate levels of CLV1 signaling activity. Rather than complete loss-of-function mutations that cause uncontrollable expansion, these partial-function alleles provide sufficient signaling to maintain control while allowing greater meristem expansion and increased flower number.
3Manufacturing precision
If CRISPR-Cas editing is used to create LRR-RLK mutations, then meristem size control is improved, but the editing process complexity increases
Solution Approach 1:
The patent applies the extraction principle by isolating and modifying specific functional domains of the LRR-RLK genes using CRISPR-Cas editing. Rather than attempting to edit entire genes, the system targets specific exons or domains responsible for kinase activity or receptor function, simplifying the editing process while achieving precise functional outcomes.
Data Source
AI summary
This invention relates to compositions and methods for modifying a Leucine Rich Repeat Receptor Like Protein Kinase (LRR-RLK) gene in plants to increase kernel row number. The invention further relates to plants having increased kernel row number produced using the methods and compositions of the invention.