@article{fdi:010088702, title = {{T}he mi{RNA}822 loaded by {ARGONAUTE}9 modulates the monosporic female gametogenesis in {A}rabidopsis thaliana}, author = {{T}ovar-{A}guilar, {A}. and {G}rimanelli, {D}aniel and {A}costa-{G}arcía, {G}. and {V}ielle-{C}alzada, {J}. {P}. and {B}adillo-{C}orona, {J}. {A}. and {D}urán-{F}igueroa, {N}.}, editor = {}, language = {{ENG}}, abstract = {{I}n the ovule of flowering plants, the establishment of the haploid generation occurs when a somatic cell differentiates into a megaspore mother cell ({MMC}) and initiates meiosis. {A}s most flowering plants, {A}rabidopsis thaliana ({A}rabidopsis) undergoes a monosporic type of gametogenesis as three meiotically derived cells degenerate, and a single one-the functional megaspore ({FM}), divides mitotically to form the female gametophyte. {T}he genetic basis and molecular mechanisms that control monosporic gametophyte development remain largely unknown. {H}ere, we show that {A}rabidopsis plants carrying loss-of-function mutations in the mi{R}822, give rise to extranumerary surviving megaspores that acquire a {FM} identity and divides without giving rise to differentiated female gametophytes. {T}he overexpression of three mi{R}822 putative target genes encoding cysteine/histidine-rich {C}1 ({DC}1) domain proteins, {A}t5g02350, {A}t5g02330 and {A}t2g13900 results in defects equivalent to those found in mutant mir822 plants. {T}he three mi{R}822 targets genes are overexpressed in ago9 mutant ovules, suggesting that mi{R}822 acts through an {AGO}9-dependent pathway to negatively regulate {DC}1 domain proteins and restricts the survival of meiotically derived cells to a single megaspore. {O}ur results identify a mechanism mediated by the {AGO}9-mi{R}822 complex that modulates monosporic female gametogenesis in {A}rabidopsis thaliana.}, keywords = {mi{RNA} ; {F}emale gametogenesis ; {ARGONAUTE} ; {A}rabidopsis ; {M}onosporic ; development}, booktitle = {}, journal = {{P}lant {R}eproduction}, volume = {[{E}arly access]}, numero = {}, pages = {[16 p.]}, ISSN = {2194-7953}, year = {2023}, DOI = {10.1007/s00497-023-00487-2}, URL = {https://www.documentation.ird.fr/hor/fdi:010088702}, }