Os01g0169800

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FIB plays a pivotal role in IAA biosynthesis in rice and that auxin biosynthesis, transport and sensitivity are closely interrelated. [1]

Annotated Information

Function

Measurement of auxin content and auxin responses in fib. (from reference [1]).

IAA content in fib-1 was reduced to about half of the wild-type in both shoot and root apices. FIB plays a pivotal role in rice IAA biosynthesis similar to that of TAA1 and VT2 in Arabidopsis and maize, respectively. The application of IAA enhanced lateral and crown root formation in a dose-dependent manner in both the wild-type and fib-1. However, the abnormal phenotypes of the fib mutant could not be fully rescued. Although the fib-1 seminal root was about three times longer than the wild-type under IAA-free conditions, the application of IAA resulted in a shorter fib-1 seminal root than the wild-type. Root growth inhibition was first observed at a dose as low as 0.003 μm IAA in fib-1, while the growth of wild-type roots was inhibited at doses higher than 0.09 μm IAA. These results indicate that fib is more sensitive to IAA than the wild-type. It is well known that NAA and 2,4-D are good substrates for auxin efflux and influx carriers, respectively [2]. fib-1 also showed higher sensitivity to 2,4-D than the wild-type, but a higher sensitivity was not observed in NAA treatment. These different sensitivities of fib to IAA, 2,4-D and NAA indicated the possibility that fib is defective in auxin polar transport.

Analysis of polar auxin transport (PAT) activity in fib and PAT inhibition by naphthyl-phtalamic acid (NPA) treatment. (from reference [1]).

In the fib-1 inflorescence stem (rachis), basipetal auxin transport decreased to ~10% of the wild-type, and acropetal auxin transport was suppressed in the roots to ~28% of the wild-type. Therefore, it is clear that PAT activity is reduced in both above- and below-ground parts of the fib-1 mutant. To test whether fib phenotypes were mimicked by PAT inhibition in the wild-type. Wild-type plants treated with NPA showed abnormal phyllotaxis, disrupted vascular tissue differentiation, decreased crown and lateral roots and defective root gravitropism. All of these abnormalities were observed in fib. Thus, the fib phenotypes are considered to be due, at least in part, to defects in PAT. The application of 7.29 μm IAA alone caused a 42% inhibition of wild-type seminal root growth, while simultaneous application of IAA and NPA resulted in more severe inhibition (68%). This result indicated that NPA application, which resulted in reduced PAT activity, enhanced sensitivity to auxin.

Mutation

Phenotypes of fib plants. (from reference [1]).

In the vegetative shoots, fib showed an extremely dwarf phenotype together with narrow and adaxially rolled short leaves. The leaf blade was highly bent at the lamina joint. In the reproductive phase, fib formed small inflorescences, about half of the wild-type, and set a reduced number of spikelets, about a tenth of the wild-type. In flowers, partial or complete homeotic conversion of lodicules (equivalent to petals) into stamens occurred frequently. In roots, fib plants lacked gravitropism and developed the seminal root two- to three-fold longer than the wild-type, but formed fewer crown and lateral roots than the wild-type. Cross-sections of leaf primordia revealed a significantly reduced number of vascular bundles. Abnormal development was also observed in the transverse veins of the leaf blade, such as aberrant orientation and fragmentation. In addition, fib plants showed aberrant phyllotaxy that deviated from the normal distichous one. These phenotypes suggested the possibility that fib mutants were defective in auxin-related processes as many of these phenotypes resembled those found in auxin-related mutants of rice and Arabidopsis [3][4][5][6][7][8].

Expression

Analysis of FIB expression. (from reference [1]).

FIB was expressed in all organs examined, including the embryo, shoot apex, leaf, inflorescence, flower and root, throughout the life cycle, suggesting a fundamental function for FIB in rice development. This expression pattern corresponded to the pleiotropic phenotypes of fib mutants. In the vegetative shoot apex, FIB was expressed predominantly in parenchymatous cells of vascular tissues and epidermal cells of leaf primordia. These signals were detected from the incipient stage of the leaf primordia and appeared clearly in the P3 leaf primordium. Tao et al. [9] reported the expression pattern of TAA1 in developing Arabidopsis embryos, in which the signals were detected in the developing vasculature as well as in the L1 layer of the presumptive shoot apical meristem and the adaxial epidermis of the developing cotyledons. The similar expression pattern between FIB and TAA1 supported the idea that FIB had functional similarity to TAA1.

Labs working on this gene

1. Graduate School of Agricultural and Life Sciences, University of Tokyo, Tokyo, Japan 2. Department of Biological Sciences, Tokyo Metropolitan University, Tokyo, Japan 3. Bioscience and Biotechnology Center, Nagoya University, Nagoya, Japan 4. School of Agricultural Regional Vitalization, Kibi International University, Minamiawaji, Japan 5. National Institute for Basic Biology, Okazaki, Japan 6. Maebashi Institute of Technology, Maebashi, Japan 7. National Institute of Agrobiological Sciences, Tsukuba, Japan

References

  1. 1.0 1.1 1.2 1.3 1.4 Yoshikawa, T., Ito, M., Sumikura, T., Nakayama, A., Nishimura, T., Kitano, H., Yamaguchi, I., Koshiba, T., Hibara, K.-I., Nagato, Y. and Itoh, J.-I. (2014), The rice FISH BONE gene encodes a tryptophan aminotransferase, which affects pleiotropic auxin-related processes. The Plant Journal, 78: 927–936.
  2. Delbarre, A., Muller, P., Imhoff, V. and Guern, J. (1996) Comparison of mechanisms controlling uptake and accumulation of 2,4-dichlorophenoxy acetic acid, naphthalene-1-acetic acid, and indole-3-acetic acid in suspension-cultured tobacco cells. Planta, 198, 532–541.
  3. Vernoux, T., Kronenberger, J., Grandjean, O., Laufs, P. and Traas, J. (2000) PIN-FORMED 1 regulates cell fate at the periphery of the shoot apical meristem. Development, 127, 5157–5165.
  4. Scarpella, E., Marcos, D., Friml, J. and Berleth, T. (2006) Control of leaf vascular patterning by polar auxin transport. Genes Dev. 20, 1015–1027.
  5. Bainbridge, K., Guyomarc'h, S., Bayer, E., Swarup, R., Bennett, M., Mandel, T. and Kuhlemeier, C. (2008) Auxin influx carriers stabilize phyllotactic patterning. Genes Dev. 22, 810–823.
  6. Kitomi, Y., Ogawa, A., Kitano, H. and Inukai, Y. (2008) CRL4 regulates crown root formation through auxin transport in rice. Plant Root, 2, 19–28.
  7. Křeček, P., Skůpa, P., Libus, J., Naramoto, S., Tejos, R., Friml, J. and Zažímalová, E. (2009) The PIN-formed (PIN) protein family of auxin transporters. Genome Biol. 10(12), 249.
  8. Mei, Y., Jia, W.J., Chu, Y.J. and Xue, H.W. (2012) Arabidopsis phosphatidylinositol monophosphate 5-kinase 2 is involved in root gravitropism through regulation of polar auxin transport by affecting the cycling of PIN proteins. Cell Res. 22, 581–597.
  9. Tao, Y., Ferrer, J.L., Ljung, K. et al. (2008) Rapid synthesis of auxin via a new tryptophan-dependent pathway is required for shade avoidance in plants. Cell, 133(1), 164–176.

Structured Information