The DOI matches its Crossref record; 30 of the 30 references it cites were found in a registry or an index.
The auxin-insensitive bodenlos mutation affects primary root formation and apical-basal patterning in the Arabidopsis embryo
Abstract
In Arabidopsis embryogenesis, the primary root meristem originates from descendants of both the apical and the basal daughter cell of the zygote. We have isolated a mutant of a new gene named BODENLOS (BDL) in which the primary root meristem is not formed whereas post- embryonic roots develop and bdl seedlings give rise to fertile adult plants. Some bdl seedlings lacked not only the root but also the hypocotyl, thus resembling monopteros (mp) seedlings. In addition, bdl seedlings were insensitive to the auxin analogue 2,4-D, as determined by comparison with auxin resistant1 (axr1) seedlings. bdl embryos deviated from normal development as early as the two-cell stage at which the apical daughter cell of the zygote had divided horizontally instead of vertically. Subsequently, the uppermost derivative of the basal daughter cell, which is normally destined to become the hypophysis, divided abnormally and failed to generate the quiescent centre of the root meristem and the central root cap. We also analysed double mutants. bdl mp embryos closely resembled the two single mutants, bdl and mp, at early stages, while bdl mp seedlings essentially consisted of hypocotyl but did form primary leaves. bdl axr1 embryos approached the mp phenotype at later stages, and bdl axr1 seedlings resembled mp seedlings. Our results suggest that BDL is involved in auxin-mediated processes of apicalbasal patterning in the Arabidopsis embryo.
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Metadata
- Authors
- Hamann, T., Mayer, U., & Jürgens, G.
- Venue
- Development
- Publisher
- The Company of Biologists
- Published
- 1999-04-01
- Volume
- 126
- Issue
- 7
- Pages
- 1387-1395
- ISSN
- 0950-1991 (ISSN-L)
- 1477-9129
- OpenAlex
- W2121956436
- Cited by
- 388
- References
- 30
- FWCI
- 23.48
- Type
- journal article
- Language
- en
- Open access
- closed
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