Ectopic expression of HaHB4 in transgenic soybean leaves enhances the asymmetric formation of secondary vein pairs.
    Annals of Botany

    LAX2 modulates leaf lateral- vein symmetry and represses xylem development

    botanyone
    November 6, 2017
    2 min read

    This work opens a novel perspective for the study of vascular pattering in crops and its potential impact in the physiology of economically relevant plants.

    The characterization of transgenic plants expressing the sunflower transcription factor HaHB4 uncovered a new role for the lateral auxin influx carrier LAX2 in venation patterning and xylem vasculature development. Most of single and multiple mutants for AUX/LAX genes presented an enhanced asymmetry in the venation patterning.

    Ectopic expression of HaHB4 in transgenic soybean leaves enhances the asymmetric formation of secondary vein pairs.
    Ectopic expression of HaHB4 in transgenic soybean leaves enhances the asymmetric formation of secondary vein pairs. (A) Illustrative photographs of the terminal foliole. White arrowheads indicate development start sites of different vein pairs. Scale bar represents 3 cm. (B) Fraction of asymmetric attachment sites compared to the total lateral vein pairs in the foliole. A total of three replicates were used to calculate the s.e. Differences were considered significant at *P < 0·05 (Student’s t-test). (C) GmLAX transcript levels detected by RT-qPCR using total RNA isolated from soybean third foliole of a fully expanded leaf. Measurements were taken on the terminal foliole from the last fully developed leaf corresponding to a 30-d-old soybean plant (V7 stage). Error bars represent the s.e. of three independent biological replicates. Statistical significance was computed by Student’s t-test. *P < 0.05

    Additionally, Moreno-Piovano et al. show that LAX2 is a negative regulator of xylem vasculature, since the lax2 mutant exhibited increased xylem length and number of xylem cell rows. These results strongly indicated that auxin homeostasis influenced by LAX2 is required to achieve normal vascular development.

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