Abstract
An auxin-insensitive, dominant mutant, massugu2 (msg2), is caused by a mutation in one of 29 Aux/IAA genes, IAA19. Chimera genes between MSG2 promoter (pMSG2) and axr2/iaa7 or slr/iaa14 were introduced into Arabidopsis for studying specific function of each protein of the gene family. Studies of the transgenic plants show both promoter- and protein-dependent phenotypes (Muto et al., 2005, PCP 46, s208). Interestingly, plants expressing pMSG2:axr2 or pMSG2:slr lack one or both cotyledons in 30% of the population. This aberrant development of cotyledon has never been observed in msg2-1, axr2-1 or slr-1. Because pMSG2:GUS is expressed in cotyledon primordia of heart-stage embryo, ectopic expression of axr2 or slr may cause aberrant development of cotyledon. This observation implicates a mechanism which suppresses the dominant msg2-1 activity in cotyledon primordia. To investigate this hypothesis, further mutation was introduced into msg2-1 seeds and the progeny will be screened for seedlings with defective cotyledonary development.
