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Triparental plants provide direct evidence for polyspermy induced polyploidy - Nature Comm

Triparental plants provide direct evidence for polyspermy induced polyploidy - Nature Comm | Plant pathogen related | Scoop.it

It is considered an inviolable principle that sexually reproducing organisms have no more than two parents and fertilization of an egg by multiple sperm (polyspermy) is lethal in many eukaryotes. In flowering plants polyspermy has remained a hypothetical concept, due to the lack of tools to unambiguously identify and trace this event. We established a high-throughput polyspermy detection assay, which uncovered that supernumerary sperm fusion does occur in planta and can generate viable polyploid offspring. Moreover, polyspermy can give rise to seedlings with one mother and two fathers, challenging the bi-organismal concept of parentage. The polyspermy derived triploids are taller and produce bigger organs than plants resulting from a regular monospermic fertilization. In addition, we demonstrate the hybridization potential of polyspermy by instantly combining three different Arabidopsis accessions in one zygote. Our results provide direct evidence for polyspermy as a route towards polyploidy, which is considered a major plant speciation mechanism.


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Genetic dissection of Arabidopsis MAP kinase phosphatase 1-dependent PAMP-induced transcriptional responses | Journal of Experimental Botany | Oxford Academic

Genetic dissection of Arabidopsis MAP kinase phosphatase 1-dependent PAMP-induced transcriptional responses | Journal of Experimental Botany | Oxford Academic | Plant pathogen related | Scoop.it
Clustering of PAMP-induced transcripts regulated by Arabidopsis MAP kinase phosphatase 1 delineates signaling pathways that are MKP1 dependent and MPK6 dependen
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Rescooped by Yan Ma from Plants and Microbes
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Trends in Plant Science: Dancing with the Stars: An Asterid NLR Family (2017)

Trends in Plant Science: Dancing with the Stars: An Asterid NLR Family (2017) | Plant pathogen related | Scoop.it

Wu and co-workers show how a network of sensor and helper NOD-like receptor proteins (NLRs) act together to confer robust resistance to diverse plant pathogens.

Plants engage with a plethora of potential pathogens but only some of these microbial overtures lead to disease. This is due to a highly successful system of innate immune receptors that quickly identify the invader and halt its progress. Wu et al. [1] now describe new insights into the molecular choreography of plant immune receptors.

 

Our understanding of these dances began with a simple two-step. There are two partners involved: a Resistance (R) gene in the host and an Avirulence (Avr) gene in the pathogen. They dance a dance according to the gene-for-gene model and resistance is manifest only if both partners are present [2]. The simplest interpretation of the gene-for-gene model is that the R gene encodes a receptor for the product of the Avr gene [3]. In fact, most R genes encode NOD-like receptors (NLRs) that pair a central nucleotide binding domain with C-terminal leucine rich repeats (NB-LRR proteins) [4]. On the other side, most Avr genes encode effectors that are secreted by pathogens to maintain virulence by strategic manipulation of host targets. As LRRs are receptor moieties in other proteins, early models posited them as receptor domains for effectors in a direct interaction, and this simple model holds true for some resistances [5].

 

Along the way, it transpired that more sophisticated models groove to a different beat. For instance, many NLRs recognise changes induced in another host target protein that is modified enzymatically by pathogen effector (Avr) proteins [6]. Examples are also known in which decoy proteins mimic such host target proteins and facilitate recognition by NLRs [7]. Effector decoys can also be provided in cis as a fusion with the NB-LRR moieties [8]. Some NLRs dance solo, but others need two to tango. In this molecular pas-de-deux, one NLR partner is the sensor that interacts with an effector, and the other is a helper that stimulates downstream signal transduction events. These pairs interact physically, and strikingly, are typically co-located genomically in a tail-to-tail arrangement (Figure 1) [9].
 
Sensor-helper relationships also occur between non-linked NLR genes. A widespread class of NLRs called CCR proteins typified by the Nicotiana benthamiana N-required gene 1 (NRG1) and Arabidopsis activated disease resistance gene 1 (ADR1) proteins are needed for a number of sensor NLRs that recognise diverse pathogens [10]. However in this case no contact between sensor and helper has been reported. An analogous situation exists in the Solanaceae, the nightshade family, which includes tomato, eggplant and tobacco. Here a family of NLRs called NRCs (NLR required for cell death), are essential for the function of a range of sensor NLRs [11, 12]. Wu and colleagues now flesh out the details of a network of sensors and helpers in Solanaceae that may enhance the robustness of immunity signalling pathways [1].


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Tyrosine phosphorylation of the GARU E3 ubiquitin ligase promotes gibberellin signalling by preventing GID1 degradation

Tyrosine phosphorylation of the GARU E3 ubiquitin ligase promotes gibberellin signalling by preventing GID1 degradation | Plant pathogen related | Scoop.it
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BAK1 is involved in AtRALF1-induced inhibition of root cell expansion

BAK1 is involved in AtRALF1-induced inhibition of root cell expansion | Plant pathogen related | Scoop.it
Author summary The rapid alkalinization factor (RALF) is a small peptide hormone that binds to FERONIA receptor and inhibits cell expansion. The AtRALF1, a root-specific RALF isoform in Arabidopsis, opposes brassinosteroid (BR) effects on root cell elongation. To address the role of AtRALF1 and BRs in regulating cell expansion, we evaluated the response of BR signaling mutants to AtRALF1. We found that the BRI1-associated receptor kinase1 (bak1) mutants are insensitive to AtRALF1 root growth inhibition activity. Although BAK1 showed no effect on the mobilization of Ca2+ and alkalinization responses, it was required for the induction of AtRALF1-responsive genes and for the semi-dwarf phenotype of AtRALF1-overexpressing plants. Different experiments demonstrated that AtRALF1 and BAK1 interact physically in a specific manner. We also suggested that the binding of AtRALF1 to BAK1 is functional because AtRALF1 induces an increase in BAK1 phosphorylation. Our findings indicate that BAK1 plays an important role in AtRALF1 signaling.
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PNAS: Distinct regions of the Pseudomonas syringae coiled-coil effector AvrRps4 are required for activation of immunity (2012)

PNAS: Distinct regions of the Pseudomonas syringae coiled-coil effector AvrRps4 are required for activation of immunity (2012) | Plant pathogen related | Scoop.it

Gram-negative phytopathogenic bacteria translocate effector proteins into plant cells to subvert host defenses. These effectors can be recognized by plant nucleotide-binding–leucine-rich repeat immune receptors, triggering defense responses that restrict pathogen growth. AvrRps4, an effector protein from Pseudomonas syringae pv. pisi, triggers RPS4-dependent immunity in resistant accessions of Arabidopsis. To better understand the molecular basis of AvrRps4-triggered immunity, we determined the crystal structure of processed AvrRps4 (AvrRps4C, residues 134–221), revealing that it forms an antiparallel α-helical coiled coil. Structure-informed mutagenesis reveals an electronegative surface patch in AvrRps4C required for recognition by RPS4; mutations in this region can also uncouple triggering of the hypersensitive response from disease resistance. This uncoupling may result from a lower level of defense activation, sufficient for avirulence but not for triggering a hypersensitive response. Natural variation in AvrRps4 reveals distinct recognition specificities that involve a surface-exposed residue. Recently, a direct interaction between AvrRps4 and Enhanced Disease Susceptibility 1 has been implicated in activation of immunity. However, we were unable to detect direct interaction between AvrRps4 and Enhanced Disease Susceptibility 1 after coexpression in Nicotiana benthamiana or in yeast cells. How intracellular plant immune receptors activate defense upon effector perception remains an unsolved problem. The structure of AvrRps4C, and identification of functionally important residues for its activation of plant immunity, advances our understanding of these processes in a well-defined model pathosystem.


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