Auxin controls petal initiation in Arabidopsis.

Floral organs are usually arranged in concentric whorls of sepals, petals, stamens and carpels. How founder cells of these organs are specified is unknown. In Arabidopsis, the PETAL LOSS (PTL) transcription factor functions in the sepal whorl, where it restricts the size of the inter-sepal zone. Genetic evidence suggests that PTL acts to support a petal initiation signal active in the adjacent whorl. Here we aimed to characterise the signal by identifying enhancers that disrupt initiation of the remaining petals in ptl mutants. One such enhancer encodes the auxin influx protein AUX1. We have established that auxin is a direct and mobile petal initiation signal by promoting its biosynthesis in the inter-sepal zone in ptl mutant plants and restoring nearby petal initiation. Consistent with this, loss of PTL function disrupts DR5 expression, an auxin-inducible indicator of petal-initiation sites. The signalling network was extended by demonstrating that: (1) loss of RABBIT EARS (RBE) function apparently disrupts the same auxin influx process as PTL; (2) the action of AUX1 is supported by AXR4, its upstream partner in auxin influx; (3) polar auxin transport, which is controlled by PINOID (PID) and PIN-FORMED1 (PIN1), functions downstream of PTL; and (4) the action of pmd-1d, a dominant modifier of the ptl mutant phenotype, is dependent on auxin transport. Thus, loss of PTL function disrupts auxin dynamics, allowing the role of auxin in promoting petal initiation to be revealed.

PETAL LOSS is a boundary gene that inhibits growth between developing sepals in Arabidopsis thaliana.

Flower primordia are partitioned by boundaries during their early development. Such boundaries occur between whorls of organs, and also between organs within whorls. PETAL LOSS (PTL) is a trihelix transcription factor gene that is expressed in boundaries between sepal primordia in the outer whorl. Over-expression of PTL results in growth suppression suggesting that PTL normally inhibits growth between newly arising sepals. We have tested this by examining the consequences of loss of PTL function using confocal imaging. The size of the inter-sepal zone in stage 4 buds expands radially by 35-40% in ptl-1 mutants as a consequence of additional cell proliferation. There is no change in the size of PTL-expressing cells. PTL expression does not overlap with the sites of petal initiation identified using the DR5 auxin response reporter. The latter are closer to the centre of the flower. Thus the consequence of loss of PTL function on petal initiation is indirect, perhaps through interference with a mobile petal-initiation signal or movement of the PTL protein. CUP-SHAPED COTYLEDON (CUC) genes are also involved in defining inter-sepal boundaries. However, genetic studies combining ptl with loss of cuc1 function, and gain of CUC function in extra early petals-1 (miR164c) mutants, have revealed that CUC and PTL act differently. CUC suppresses growth of sepal tissues from the boundary region whereas PTL acts to keep the size of the boundary in check.

Magnetic Resonance Imaging of Non-Puerperal Complete Uterine Inversion.

Uterine inversion is shortly described as the indentation and depression of the fundic area extending downwards up to the different levels of the birth canal till vaginal opening. Clinical diagnosis of uterine inversion is difficult due to its non-specific symptoms and physical examination. Ultrasonography is the most practical modality for radiological evaluation, but it is inadequate to determine the exact nature of this condition and making the differential diagnosis. In this case, we present the main MRI findings of non-puerperal complete uterine inversion caused by a giant leiomyoma.

PETAL LOSS, a trihelix transcription factor gene, regulates perianth architecture in the Arabidopsis flower.

Perianth development is specifically disrupted in mutants of the PETAL LOSS (PTL) gene, particularly petal initiation and orientation. We have cloned PTL and show that it encodes a plant-specific trihelix transcription factor, one of a family previously known only as regulators of light-controlled genes. PTL transcripts were detected in the early-developing flower, in four zones between the initiating sepals and in their developing margins. Strong misexpression of PTL in a range of tissues universally results in inhibition of growth, indicating that its normal role is to suppress growth between initiating sepals, ensuring that they remain separate. Consistent with this, sepals are sometimes fused in ptl single mutants, but much more frequently in double mutants with either of the organ boundary genes cup-shaped cotyledon1 or 2. Expression of PTL within the newly arising sepals is apparently prevented by the PINOID auxin-response gene. Surprisingly, PTL expression could not be detected in petals during the early stages of their development, so petal defects associated with PTL loss of function may be indirect, perhaps involving disruption to signalling processes caused by overgrowth in the region. PTL-driven reporter gene expression was also detected at later stages in the margins of expanding sepals, petals and stamens, and in the leaf margins; thus, PTL may redundantly dampen lateral outgrowth of these organs, helping define their final shape.