LRR-RLK Allele Editing for Larger Maize Meristems
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Solution Overview
Problem
Existing methods for modifying meristem size in plants, particularly in maize, to increase kernel row number and yield are limited, 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 meristem organization becomes disorganized and aberrant growth occurs
Solution Approach 1:
The invention changes the functional state of the LRR-RLK protein by introducing specific mutations (kinase-dead, dominant-negative, or loss-of-function alleles) that alter its signaling capacity. This parameter change in protein function allows meristem expansion without the pathological disorganization seen in complete loss-of-function mutants, achieving a balanced state that increases kernel row number while maintaining meristem organization.
2Quantity of substance
If LRR-RLK signaling is completely inhibited to expand meristem size, then flower number increases, but plant growth becomes aberrant and disorganized
Solution Approach 1:
The invention applies partial inhibition of LRR-RLK signaling through kinase-dead or dominant-negative alleles that retain some signaling capacity. This partial action is sufficient to expand meristem size and increase flower number, but not so complete as to cause aberrant growth disorganization, achieving the desired effect with optimized intensity.
3Volume of stationary object
If dominant-negative LRR-RLK alleles are introduced to compete with wildtype receptors, then meristem size increases, but signaling specificity may be compromised
Solution Approach 1:
The dominant-negative LRR-RLK allele acts as an intermediary that competes with wildtype receptors for ligand binding but cannot transmit the full signaling cascade. This intermediary protein allows controlled modulation of signaling intensity while maintaining some degree of specificity through its structured interaction with ligands and downstream components.
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 kemel row number produced using the methods and compositions of the invention.


