| The Shoot Apical Meristem (SAM) is the postembryonic source of aboveground plant organs. Many genes are involved in coordinating the complex organization and functioning of the SAM, but only the SHOOTMERISTEMLESS (STM) gene product is known to be both necessary and sufficient to make a SAM. The studies presented in this thesis provide new insights into how STM functions and thus contribute to our understanding of plant development. First I raised antibodies that specifically recognize the STM protein. Anti-STM immunolocalizations reveal that the STM protein is found within the presumptive shoot apex, from early embryogenesis through adult development. Next I looked at STM protein expression throughout early development in various SAM mutants. These analyses reveal that mutating other genes that affect SAM functioning changes the localization of STM.; A series of rescue projects were undertaken in order to understand the relative contribution of STM to the peripheral zone (PZ) and the central zone (CZ) of the SAM. Expression of STM in only the PZ of an stm individual restored full wild-type meristem capacity to stm transgenic plants. STM mRNA was detected at wild-type levels in the PZ of rescued shootmeristemless plants, but STM protein was found at wild-type levels in the PZ and the CZ. I propose that STM moves from the PZ to the CZ providing necessary STM function throughout the SAM and yielding full rescue of the stm phenotype. I also show that KNAT1, KNAT2, and an STM:GUS protein fusion are not capable of fully rescuing the stm phenotype when expressed in the PZ of the SAM. |
