MALE STERILITY 35 (dehiscence mutant)

We have isolated and characterised an anther dehiscence mutant, ms35/AtMYB26 [Steiner-Lange, S., et al., (2003)]. The lack of dehiscence is due, at least in part, to impaired deposition of endothecial secondary wall thickening [Dawson, J., et al., 1999]. This mutant cannot be rescued by Jasmonic Acid (JA) application and the role of the AtMYB26 gene in anther dehiscence is thought to be independent of the JA pathway.

Pollen development in the ms35 mutant

Anther dehiscence, is a multi-step process which includes the lytic opening of a longitudinal line of weakness in the epidermis, known as the stomium, and retraction of the anther wall to widen the stomium and permit pollen release. During microspore maturation, cellulose and lignified thickenings are deposited in the endothecium. The cells of the stomium and circular cell cluster are then enzymatically lysed.

The endothecium is thought to be critical in generating the forces required for dehiscence. Firstly, swelling of the endothecium cells provides an inwardly directed force causing the weakened stomium to rupture. Then, desiccation of the endothecium causes differential shrinkage of thickened and unthickened parts of the cell wall, resulting in an outward bending force leading to retraction of the anther wall and full opening of the stomium.

Anther and pollen development follows the same pattern in Ler (wt) and ms35. Lysis of the cells forming the stomium appears to occur normally (arrow), leaving no bridge between the epidermal/endothecial cells on either side of the stomium.

Wild type anther- dehiscence and pollen release occurs.

ms35 mutant anther- no dehiscence of the anther and pollen fails to be released.

However, wall thickenings are not formed in the ms35 endothecium, resulting in the endothecial cells becoming flattened and distorted. The lack of thickening means that the outward bending of the anther wall fails to occur, the endothecial cells collapse and the anther fails to open. However, the pattern of lignification in the vascular tissue of the anthers, stems and leaves are the same in wt and ms35 plants. Therefore, the ms35 mutation, directly or indirectly, affects secondary wall deposition specifically in the endothecium.