pin mutants have greatly impaired fertility

pin mutants have greatly impaired fertility click here and striking sporophytic defects that are similar to published defects arising from treatment with auxin transport inhibitors. Our results show that PIN proteins are conserved auxin transport facilitators. To clarify the roles of auxin in moss gametophore development, we grew colonies on medium supplemented with auxins that have different biochemical properties: indoleacetic acid (IAA), naphthylacetic acid (NAA), and 2,4-dichlorophenoxyacetic acid (2,4-D). Although weak effects were seen with the native auxin IAA (Figure S1 available online), a spectrum of phenotypes of lesser-to-greater severity was observed in treatments

with NAA and 2,4-D and was classified into five phenotypic classes, classes I–V (Figures 1A and S1). An increased frequency of more-severe phenotypes correlated with increasing auxin concentrations (Figure S1C). When grown on lower auxin concentrations (e.g., 100 nM NAA, 1 μM 2,4-D), class I and class II shoots were prevalent. Class I shoots appeared similar to controls, but the zone of rhizoid emergence was displaced apically, as in previous reports [47, 48 and 49]. Class II shoots (seen in 2,4-D treatments) were elongated and had more leaves than controls (Figures 1A, 1C, S1A,

and S1D). Class III shoots were stunted, producing fewer leaves than IDO inhibitor untreated controls (Figures 1A, 1B, and S1D), and leaves were narrow with fewer, longer cells than untreated controls (Figures 1C, S1B, and S1D). In class IV shoots, leaf outgrowth was suppressed, and gametophores comprised a raspberry-like dome of cells above a zone of rhizoid emergence (Figure 1A). Confocal microscopy revealed

a spiral of successively larger leaf progenitor cells emanating from the apical cell, thus demonstrating its continued activity (Figure 1B). The strongest effect of auxin was revealed in class V shoots, which lost apical cell function. Shoots terminated with irregularly shaped cells, or rhizoids, consistent with previous reports [47 and 49] (Figure 1B). These data suggest that accumulation of auxin in shoots triggers diverse developmental effects at different threshold Sclareol levels. Notably, auxin accumulation causes defects in meristem function, leaf initiation, and oriented leaf growth. By analogy to flowering plants, we hypothesized that gametophore development is normally driven by changes in the auxin distribution within tissues, which was disrupted by adding exogenous auxin. We reasoned that such changes might occur by a conserved transport-dependent mechanism. To test this hypothesis, we analyzed the effect on gametophore development of the compounds 1-N-naphthylphthalamic acid (NPA) and naringenen (Nar), which are potent PATIs in angiosperms.

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