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. 2009 May 8;5(5):e1000476. doi: 10.1371/journal.pgen.1000476

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This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration, which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

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(A) Leaves of non-mutant maize leaves are much wider than the (B) narrow leaves formed on the short plants of asc1-2 mutants. The male inflorescence (tassel) of asc1-2 mutants form small, sterile branches devoid of florets (C), whereas non-mutant tassels are larger, and the numerous branches form multiple, pollen-bearing florets (D). Longitudinal sections of the shoot apex of (E) non-mutant and (F) asc1-2 mutant seedlings reveal a greatly reduced SAM size in the mutant apex. Transverse sections reveal the narrow leaf asc1 mutant phenotype. Note that the margins (white arrow) of the fourth numbered leaf completely overlap the shoot apex in non-mutant seedlings (G), but are severely truncated in the asc1-1 mutant (H). Development of leaf vascular bundles is also disrupted in asc1 mutant seedlings. The number and size of the xylem (x) and phloem (p) elements in the midvein of the sixth non-mutant leaf (I) are diminished in equivalent leaves of asc1-1 mutant seedlings (J). As compared to non-mutant siblings (K), major defects in stomatal (arrows) patterning and spacing are observed in the leaf epidermis of asc1-1 mutants (L), asc1-2 mutants (M), and in mutant progeny obtained from crosses between asc1-M1 and asc1-M2 heterozygotes, which fail to complement.