Cysteine-rich receptor-like kinase and MADS-box co-regulation of programmed cell death drives apical spikelet degeneration in wheat.

Spikelet degeneration and pollen sterility are primary constraints on grain set in wheat (Triticum aestivum L.), yet their molecular underpinnings remain poorly defined. We characterized degenerated spikelets 1 (ds1), a wheat mutant displaying apical spikelet degeneration and middle spikelet sterility. Relative to wild type, ds1 exhibited a 17.0% reduction in spike length, an 88.8% decline in grain-bearing spikelets, and a 93.6% drop in grain number per spike. Fine mapping localized the causal locus to chromosome 3BL, where DS1, encoding a cysteine-rich receptor-like kinase, was identified as the causal gene and found to be strongly downregulated in degenerated spikelets. Concordantly, multiple MADS-box transcription factors were transcriptionally suppressed in ds1 degenerated spikelets. Histological analysis revealed anther shrinkage, disrupted boundaries between anther wall layers, and defective cuticle structure. Excessive reactive oxygen species accumulated in the anther outer wall, triggering programmed cell death. Loss of cuticular wax on the anther surface, combined with premature tapetal degradation, produced hollow anther locules, aberrant pollen exine layering, and failure of microspore maturation, culminating in sterility. Together, these findings demonstrate that coordinated regulation of PCD, tapetal development, and pollen exine formation is indispensable for normal spikelet and floret development in wheat.