Satoh N, Hong S K, Nishimura A, Matsuoka M, Kitano H, Nagato Y
Graduate School of Agricultural and Life Sciences, University of Tokyo, Tokyo 113-8657, Japan.
Development. 1999 Aug;126(16):3629-36. doi: 10.1242/dev.126.16.3629.
The regulatory mechanism of shoot apical meristem (SAM) initiation is an important subject in developmental plant biology. We characterized nine recessive mutations derived from four independent loci (SHL1-SHL4) causing the deletion of the SAM. Radicles were produced in these mutant embryos. Concomitant with the loss of SAM, two embryo-specific organs, coleoptile and epiblast, were lost, but the scutellum was formed normally. Therefore, differentiation of radicle and scutellum is regulated independently of SAM, but that of coleoptile and epiblast may depend on SAM. Regeneration experiments using adventitious shoots from the scutellum-derived calli showed that no adventitious shoots were regenerated in any shl mutant. However, small adventitious leaves were observed in both mutant and wild-type calli, but they soon became necrotic and showed no extensive growth. Thus, leaf primordia can initiate in the absence of SAM, but their extensive growth requires the SAM. An in situ hybridization experiment using a rice homeobox gene, OSH1, as a probe revealed that shl1 and shl2 modified the expression domain of OSH1, but normal expression of OSH1 was observed in shl3 and shl4 embryos. Accordingly, SHL1 and SHL2 function upstream of OSH1, and SHL3 and SHL4 downstream or independently of OSH1. These shl mutants are useful for elucidating the genetic program driving SAM initiation and for unraveling the interrelationships among various organs in grass embryos.
茎尖分生组织（SAM）起始的调控机制是植物发育生物学中的一个重要课题。我们鉴定了来自四个独立位点（SHL1-SHL4）的九个隐性突变，这些突变导致SAM缺失。在这些突变胚胎中产生了胚根。与SAM的丧失相伴，两个胚胎特异性器官，胚芽鞘和外胚叶丧失，但盾片正常形成。因此，胚根和盾片的分化独立于SAM进行调控，但胚芽鞘和外胚叶的分化可能依赖于SAM。利用来自盾片愈伤组织的不定芽进行的再生实验表明，在任何shl突变体中都没有再生出不定芽。然而，在突变体和野生型愈伤组织中都观察到了小的不定叶，但它们很快坏死，没有广泛生长。因此，叶原基可以在没有SAM的情况下起始，但其广泛生长需要SAM。使用水稻同源异型框基因OSH1作为探针的原位杂交实验表明，shl1和shl2改变了OSH1的表达域，但在shl3和shl4胚胎中观察到OSH1的正常表达。因此，SHL1和SHL2在OSH1的上游起作用，而SHL3和SHL4在OSH1的下游或独立于OSH1起作用。这些shl突变体对于阐明驱动SAM起始的遗传程序以及揭示禾本科植物胚胎中各种器官之间的相互关系很有用。
