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Branching/tillering is a critical process for plant architecture and grain yield. However, Branching is intricately controlled by both endogenous and environmental factors. The underlying mechanisms of tillering in wheat remain poorly understood. In this study, we identified Less Tiller 1 (LT1) as a novel regulator of wheat tillering using an enhanced bulked segregant analysis (BSA) method, uni-BSA. This method effectively reduces alignment noise caused by the high repetitive sequence content in the wheat genome. Loss-of-function of LT1 results in fewer tillers due to defects in axillary meristem initiation and bud outgrowth. We mapped LT1 to a 6 Mb region on the chromosome 2D short arm and validated a nucleotide-binding (NB) domain encoding gene as LT1 using CRISPR/Cas9. Furthermore, the lower sucrose concentration in the shoot bases of lt1 might result in inadequate bud outgrowth due to disturbances in the sucrose biosynthesis pathways. Co-expression analysis suggests that LT1 controls tillering by regulating TaROX/TaLAX1, the ortholog of the Arabidopsis tiller regulator REGULATOR OF AXILLARY MERISTEM FORMATION (ROX) or the rice axillary meristem regulator LAX PANICLE1 (LAX1). This study not only offers a novel genetic resource for cultivating optimal plant architecture but also underscores the importance of our innovative BSA method. This uni-BSA method enables the swift and precise identification of pivotal genes associated with significant agronomic traits, thereby hastening gene cloning and crop breeding processes in wheat. [ABSTRACT FROM AUTHOR]

Background: Disrupted-in-schizophrenia 1 (DISC1) is a promising candidate susceptibility gene for psychiatric disorders, including schizophrenia, bipolar disorder and major depression. Several previous studies reported that mice with A/-ethyl-A/-nitrosourea (ENU)-induced L100P mutation in Disc1 showed some schizophrenia-related behavioral phenotypes. This line originally carried several thousands of ENU-induced point mutations in the C57BL/6 J strain and single nucleotide polymorphisms (SNPs) from the DBA/2 J inbred strain. Methods: To investigate the effect of Disc1 L100P, background mutations and SNPs on phenotypic characterization, we performed behavioral analyses to better understand phenotypes of Disc1 L100P mice and comprehensive genetic analyses using whole-exome resequencing and SNP panels to map ENU-induced mutations and strain-specific SNPs, respectively. Results: We found no differences in spontaneous or methamphetamine-induced locomotor activity, sociability or social novelty preference among Disc1 L100P/L100P, L100P/+ mutants and wild-type littermates. Whole-exome resequencing of the original G1 mouse identified 117 ENU-induced variants, including Disc1 L100P per se. Two females and three males from the congenic L100P strain after backcrossing to C57BL/6 J were deposited to RIKEN BioResource Center in 2008. We genotyped them with DBA/2 J x C57BL/6 J SNPs and found a number of the checked SNPs still remained. Conclusion: These results suggest that causal attribution of the discrepancy in behavioral variance phenotypes to the Disc1 L100P mutant mouse line existing among different research groups needs to be cautiously investigated in further study by taking into account the effect(s) of other ENU-induced mutations and/or SNPs from DBA/2 J. [ABSTRACT FROM AUTHOR]