Abstract: 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 . |