A cellular mechanism underlying the restoration of thermo/photoperiod-sensitive genic male sterility.
Mol Plant
; 14(12): 2104-2114, 2021 12 06.
Article
de En
| MEDLINE
| ID: mdl-34464765
ABSTRACT
During anther development, the transformation of the microspore into mature pollen occurs under the protection of first the tetrad wall and later the pollen wall. Mutations in genes involved in this wall transition often lead to microspore rupture and male sterility; some such mutants, such as the reversible male sterile (rvms) mutant, are thermo/photoperiod-sensitive genic male sterile (P/TGMS) lines. Previous studies have shown that slow development is a general mechanism of P/TGMS fertility restoration. In this study, we identified restorer of rvms-2 (res2), which is an allele of QUARTET 3 (QRT3) encoding a polygalacturonase that shows delayed degradation of the tetrad pectin wall. We found that MS188, a tapetum-specific transcription factor essential for pollen wall formation, can activate QRT3 expression for pectin wall degradation, indicating a non-cell-autonomous pathway involved in the regulation of the cell wall transition. Further assays showed that a delay in degradation of the tetrad pectin wall is responsible for the fertility restoration of rvms and other P/TGMS lines, whereas early expression of QRT3 eliminates low temperature restoration of rvms-2 fertility. Taken together, these results suggest a likely cellular mechanism of fertility restoration in P/TGMS lines, that is, slow development during the cell wall transition of P/TGMS microspores may reduce the requirement for their wall protection and thus support their development into functional pollens, leading to restored fertility.
Mots clés
Texte intégral:
1
Collection:
01-internacional
Base de données:
MEDLINE
Sujet principal:
Photopériode
/
Arabidopsis
/
Protéines d'Arabidopsis
/
Stérilité des plantes
Type d'étude:
Diagnostic_studies
/
Prognostic_studies
Langue:
En
Journal:
Mol Plant
Sujet du journal:
BIOLOGIA MOLECULAR
/
BOTANICA
Année:
2021
Type de document:
Article
Pays d'affiliation:
Chine