Search bioRxiv⌕ Search

Biology subjects

GRIMANELLI, D.

Publications and source records attributed to GRIMANELLI, D..

2 recordsLinked to original sources

MIR822 modulates monosporic female gametogenesis through an ARGONAUTE9-dependent pathway in Arabidopsis thaliana

In the ovule of flowering plants, the establishment of the haploid generation occurs when a somatic subepidermal cell specified as the gametophytic precursor differentiates into a Megaspore Mother Cell (MMC) and initiates meiosis. As most flowering plants, Arabidopsis thaliana (Arabidopsis) undergoes a monosporic type of gametogenesis as three meiotically derived cells degenerate without further division, and a single one - the functional megaspore (FM) - divides mitotically to form the female gametophyte. The genetic basis and molecular mechanisms that control monosporic gametogenesis remain largely unknown. In Arabidopsis, ARGONAUTE proteins are involved the control of megasporogenesis. In particular, mutations in ARGONAUTE9 (AGO9) lead to the ectopic differentiation of gametic precursors that can give rise to apomeiotically derived female gametophytes. Here, we show that Arabidopsis plants carrying loss-of-function mutations in the AGO9-interacting microRNA miR822a give rise to extranumerary surviving megaspores that acquire a FM identity and divide without giving rise to differentiated female gametophytes. The overexpression of three miR822a target genes encoding Cysteine/Histidine-Rich C1 domain proteins (At5g02350, At5g02330 and At2g13900) results in defects equivalent to those found in mir822 plants. All three miR822a targets are overexpressed in ago9 mutant ovules, confirming that miR822a acts through an AGO9-dependent pathway to negatively regulate Cysteine/Histidine-Rich C1 domain proteins and restricts the survival of meiotically derived cells to a single megaspore. Our results identify a microRNA-dependent mechanism that is involved in the control of megaspore degeneration and the most prevalent form of female gametogenesis in flowering plants.

plant biology↗

AGO104 is an RdDM effector of paramutation at the maize b1 locus

Paramutation is an exception among eukaryotes, in which epigenetic information is conserved through mitosis and meiosis. It has been studied for over 70 years in maize, but the mechanisms involved are largely unknown. Previously described actors of paramutation encode components of the RNA-dependent DNA-methylation (RdDM) pathway all involved in the biogenesis of 24-nt small RNAs. However, no actor of paramutation have been identified in the effector complex of RdDM. Here, through a combination of reverse genetics, immunolocalization and immunoprecipitation (siRNA-IP) we found that ARGONAUTE104 (AGO104), AGO105 and AGO119 are members of the RdDM effector complex in maize and bind siRNAs produced from the tandem repeats required for paramutation at the b1 locus. We also showed that AGO104 is an effector of the b1 paramutation in maize. Author summaryReprogramming of epigenetic information has been described in both plants and mammals. Here, we show that maize ARGONAUTE (AGO) AGO104 and AGO105/AGO119, respectively the close homologs of A. thaliana AGO9 and AGO4, are required to enable paramutation at the b1 locus in maize. Paramutation is an epigenetic phenomenon that is stable over many generations (both mitotically and meiotically). A classic example is the booster1 (b1) gene in maize, where the weakly expressed Booster (B) allele stably decreases the expression of the Booster-Intense (B-I) allele, and changes it into a new B allele. This new B allele will in turn change B-I into new B in subsequent crosses. Previous research demonstrated that paramutation requires several proteins involved in the biosynthesis of small interfering RNAs (siRNAs) all related to the RNA-dependent DNA-methylation (RdDM) pathway. Yet, few members of the RdDM were functionally identified in maize. Here, we identify two new members of the maize RdDM pathway, and provide evidence that they are also involved in paramutation at the b1 locus.

genetics↗