Abstract
Source–sink interactions play a critical but mechanistically underexplored role in coordinating reproductive output and longevity in plants. Here, we investigated the role of FT1 , the barley homolog of the florigen FLOWERING LOCUS T ( FT ), in regulating source (leaf) and sink (inflorescence) development and metabolism. Using ft1 knock-out mutants in the spring barley cultivar Golden Promise, which carries a mutated ppd-H1 allele, and in an introgression line with a wild-type Ppd-H1 allele, we show that Ppd-H1 primarily regulates the timing of inflorescence development and flowering through FT1 , whereas variation in tiller number and leaf size is determined by the genetic background. ft1 mutants exhibited reduced determinacy of both leaf and inflorescence meristems, resulting in increased leaf and spikelet numbers and size, but severely reduced inflorescence fertility, altered senescence patterns, and significantly extended plant longevity. The ft1 mutants exhibited a strong transcriptional reprogramming of genes involved in both the light and dark reactions of photosynthesis in the leaf, alongside an upregulation of genes associated with carbon catabolism and stress responses in the leaf and inflorescence. Elevated soluble sugar and starch levels in ft1 inflorescences indicated that the impaired development and fertility of ft1 inflorescences were not caused by carbon limitation, but instead reflected a reduced sink strength. Our work reveals that FT1 coordinates the development of vegetative and reproductive meristems and organs with plant physiology and metabolism, thereby regulating source–sink relationships and balancing plant longevity with reproductive output.
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Abstract
Source–sink interactions play a critical but mechanistically underexplored role in coordinating reproductive output and longevity in plants. Here, we investigated the role of FT1, the barley homolog of the florigen FLOWERING LOCUS T (FT), in regulating source (leaf) and sink (inflorescence) development and metabolism. Using ft1 knock-out mutants in the spring barley cultivar Golden Promise, which carries a mutated ppd-H1 allele, and in an introgression line with a wild-type Ppd-H1 allele, we show that Ppd-H1 primarily regulates the timing of inflorescence development and flowering through FT1, whereas variation in tiller number and leaf size is determined by the genetic background. ft1 mutants exhibited reduced determinacy of both leaf and inflorescence meristems, resulting in increased leaf and spikelet numbers and size, but severely reduced inflorescence fertility, altered senescence patterns, and significantly extended plant longevity. The ft1 mutants exhibited a strong transcriptional reprogramming of genes involved in both the light and dark reactions of photosynthesis in the leaf, alongside an upregulation of genes associated with carbon catabolism and stress responses in the leaf and inflorescence.
Elevated soluble sugar and starch levels in ft1 inflorescences indicated that the impaired development and fertility of ft1 inflorescences were not caused by carbon limitation, but instead reflected a reduced sink strength. Our work reveals that FT1 coordinates the development of vegetative and reproductive meristems and organs with plant physiology and metabolism, thereby regulating source–sink relationships and balancing plant longevity with reproductive output.
Competing Interest Statement
The authors have declared no competing interest.
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