DEK219 and HSF17 Collaboratively Regulate the Kernel Length in Maize.

Area of Science:

• Plant genetics and molecular biology
• Crop science
• Maize (Zea mays L.) research

Background:

• Kernel length is a key factor in determining maize yield.
• Limited knowledge exists regarding the genetic mechanisms controlling maize kernel length.
• The maize mutant defective kernel219 (dek219), encoding DICER-LIKE1, affects miRNA biogenesis and kernel length.

Purpose of the Study:

• To investigate the role of DEK219 in regulating maize kernel length.
• To identify genes and transcription factors involved in DEK219-mediated kernel length control.
• To elucidate the molecular mechanism by which DEK219 influences kernel development.

Main Methods:

• Phenotypic analysis of the dek219 mutant.
• miRNA-target gene prediction, expression analysis, and correlation analysis.
• Transient expression analysis and electrophoretic mobility shift assay (EMSA).

Main Results:

• The dek219 mutant consistently shows reduced kernel length.
• Nine transcription factors were identified as potential regulators under DEK219 control.
• HEAT SHOCK TRANSCRIPTION FACTOR17 (HSF17) was significantly upregulated and identified as a negative regulator, inhibiting DEFECTIVE ENDOSPERM18 (DE18) expression, leading to increased kernel length in hsf17 mutants.

Conclusions:

• DEK219 plays a role in maize kernel length regulation, potentially by modulating transcription factor activity.
• HSF17 acts as a negative regulator of maize kernel length by inhibiting DE18.
• This research provides insights into maize kernel development and offers genetic resources for breeding improved varieties.