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When sun plants, such as  Arabidopsis thaliana,   are under canopy shade, elongation of stems/petioles will be induced as one of the most prominent responses. Plant hormones mediate the elongation growth. However, how environmental and hormonal signals are translated into cell expansion activity that leads to the elongation growth remains elusive. Through forward genetic study, we identified   s hade  av oidance2  ( sav2 ) mutant, which contains a P287L mutation in β‐TUBULIN 4. Cortical microtubules (cMTs) play a key role in anisotropic cell growth. Hypocotyls of  sav2  are wild type‐like in white light, but are short and highly swollen in shade and dark. We showed that shade not only induces cMT rearrangement, but also affects cMT stability and dynamics of plus ends. Even though auxin and brassinosteroids are required for shade‐induced hypocotyl elongation, they had little effect on shade‐induced rearrangement of cMTs. Blocking auxin transport suppressed dark phenotypes of   sav2 , while overexpressing   EB1b‐GFP,   a microtubule plus‐end binding protein ,   rescued  sav2  in both shade and dark, suggesting that  tub4 P287L    represents a unique type of tubulin mutation that does not affect cMT function in supporting cell elongation, but may affect the ability of cMTs to respond properly to growth promoting stimuli.

Characterization of tub4 P287L , a β‐tubulin mutant, revealed new aspects of microtubule regulation in shade