LATERAL FLORET 2 encoding a sucrose non‐fermenting 2 chromatin remodeling factor regulates axillary meristem of spikelet development in rice (Oryza sativa)

Summary The spikelet, a unique inflorescence unit of grasses such as rice ( Oryza sativa ), possesses developmental regulatory mechanisms that require further exploration. In this study, we identified a mutant named lateral floret2 ( lf2 ), which exhibited abnormalities in spikelet development. The lf2 mutants produced lateral florets within the axils of sterile lemmas and/or lateral spikelets within the axils of rudimentary glumes. Additionally, elongated rudimentary glumes and lemma‐like sterile lemmas were observed in these mutant spikelets. Notably, these ectopic lateral florets or spikelets bored normal floral organs similar to the wild‐type terminal florets. The LF2 gene encoded a SWI/SNF-related, matrix-associated, actin-dependent regulator of chromatin, subfamily A-like 1 subfamily chromatin remodeling factor belonging to the sucrose non-fermenting 2 family and was located in the nucleus. Furthermore, we detected interactions between LF2 and several subunits of nuclear factors (NF‐Ys), and the CRISPR/Cas9‐mediated mutation of OsNF‐YA3 in transgenic plants exhibited partially similar defects in spikelet to lf2 mutant. Through correlation analyses among RNA‐Seq, reverse transcription quantitative polymerase chain reaction and chromatin immunoprecipitation (ChIP) of H3K27Me3, we identified several genes involved in the auxin synthesis/signaling pathway and organ development that exhibited differences in gene expression and histone modifications. Moreover, biochemical analyses revealed that LF2 directly targeted the G1 locus. Genetic analyses supported the hypothesis that LF2 functioned upstream of G1 to regulate sterile lemma development. Our work revealed that LF2 regulated axillary meristem initiation by modulating the auxin synthesis and signaling pathway, and determined sterile lemma identity by maintaining the expression of the G1 gene during spikelet development.