Growth discrepancy between filament and style facilitates self‐fertilization in Brandisia hancei (Paulowniaceae)

Self‐pollination has been hypothesized to be beneficial in environments where pollinators are rare as it can provide reproductive assurance. This study presents evidence for an autonomous self‐fertilization mechanism in the winter flowering plant, Brandisia hancei. To determine changes in the spatial separation of stigma and anthers, the length of style and stamens was recorded. Additionally, pollination treatments were carried out to test fruit‐set and seed production. Brandisia hancei is herkogamic in the early flowering stages. However, different growth rates of the filament and style lead to contact of stigma and anthers in the later stages, thereby facilitating self‐pollination. The highest seeds number is produced under an out‐crossing scenario but plants produce a considerable number of seeds even when purely selfed. Although pollinators are scarce, autonomous selfing alleviates the pollen limitation in B. hancei. Self‐fertilization in B. hancei seems to be an adaptive strategy to ensure reproduction when pollinators are scarce.     

AtRAD5A is a DNA translocase harboring a HIRAN domain which confers binding to branched DNA structures and is required for DNA repair in vivo

DNA lesions such as crosslinks represent obstacles for the replication machinery. Nonetheless, replication can proceed via the DNA damage tolerance pathway also known as postreplicative repair pathway. SNF2 ATPase Rad5 homologs, such as RAD5A of the model plant Arabidopsis thaliana, are important for the error‐free mode of this pathway. We able to demonstrate before, that RAD5A is a key factor in the repair of DNA crosslinks in Arabidopsis. Here, we show by in vitro analysis that AtRAD5A protein is a DNA translocase able to catalyse fork regression. Interestingly, replication forks with a gap in the leading strand are processed best, in line with its suggested function. Furthermore AtRAD5A catalyses branch migration of a Holliday junction and is furthermore not impaired by the DNA binding of a model protein, which is indicative of its ability to displace other proteins. Rad5 homologs possess HIRAN (Hip116, Rad5; N‐terminal) domains. By biochemical analysis we were able to demonstrate that the HIRAN domain variant from Arabidopsis RAD5A mediates structure selective DNA binding without the necessity for a free 3′OH group as has been shown to be required for binding of HIRAN domains in a mammalian RAD5 homolog. The biological importance of the HIRAN domain in AtRAD5A is demonstrated by our result that it is required for its function in DNA crosslink repair in vivo.     

ERIL1, the plant homologue of ERI‐1, is involved in the processing of chloroplastic rRNAs

Proteins belonging to the enhancer of RNA interference‐1 subfamily of 3′–5′ exoribonucleases participate in divergent RNA pathways. They degrade small interfering RNAs (siRNAs), thus suppressing RNA interference, and are involved in the maturation of ribosomal RNAs and the degradation of histone messenger RNAs (mRNAs). Here, we report evidence for the role of the plant homologue of these proteins, which we termed ENHANCED RNA INTERFERENCE‐1‐LIKE‐1 (ERIL1), in chloroplast function. In vitro assays with AtERIL1 proved that the conserved 3′–5′ exonuclease activity is shared among all homologues studied. Confocal microscopy revealed that ERL1, a nucleus‐encoded protein, is targeted to the chloroplast. To gain insight into its role in plants, we used Nicotiana benthamiana and Arabidopsis thaliana plants that constitutively overexpress or suppress ERIL1. In the mutant lines of both species we observed malfunctions in photosynthetic ability. Molecular analysis showed that ERIL1 participates in the processing of chloroplastic ribosomal RNAs (rRNAs). Lastly, our results suggest that the missexpression of ERIL1 may have an indirect effect on the microRNA (miRNA) pathway. Altogether our data point to an additional piece of the puzzle in the complex RNA metabolism of chloroplasts.     

Melody-free syntax and phonologically conditioned allomorphy

The paper argues that morpho-syntactic computation and phonological melody (i.e. segmental primes occurring below the skeleton) are entirely incommunicado, in both directions. That is, there is no morpho-syntactic operation, say, movement, which goes into effect only if the moved item begins with a labial.This claim is run against the specific record of phonologically conditioned allomorphy (PCA). The prediction is that only non-melody, i.e. items located at and above the skeleton, may condition allomorphy: stress, tone, size, syllable structure, rhythm and the like. On the backdrop of Paster’s (2006) and Nevins’ (2011) cross-linguistic record of PCA, challenging cases are identified: those where the trigger is melodic without there being a plausible phonological pathway from the illegal to the legal alternant. It is shown that there is a purely phonological analysis of this pattern: the arbitrary relation between the illegal and the legal alternant is encoded in the lexicon, but in one and the same lexical entry (instead of two) where the illegal item is associated to a constituent and the rescue segment floats. When the regular (associated) segment is illegal in a given phonological context, it delinks and the floating substitute attaches to the position vacated.As a consequence, a plausible case can be made to the end that morphological computation never takes into account melodic information when selecting allomorphs: all candidate patterns have a purely phonological analysis based on one single underlier. This result is evaluated in the context of the debate regarding modularity: non-modular approaches that grant exhaustive simultaneous access to morphological and phonological information overgenerate, while the modularity-restricted architecture makes the correct prediction: the access of morphological computation to phonological information is selective (excluding melody). Finally, the multiple inputs analysis (Mascaró 2007) is shown to face the same problem, albeit only for a subset of PCA patterns, the ones that are non-optimizing.     

Stability of the Encoding Plasmids and Surface Expression of CS6 Differs in Enterotoxigenic Escherichia coli (ETEC) Encoding Different Heat-Stable (ST) Enterotoxins (STh and STp)

Enterotoxigenic Escherichia coli (ETEC), one of the most common reasons of diarrhea among infants and children in developing countries, causes disease by expression of either or both of the enterotoxins heat-labile (LT) and heat-stable (ST; divided into human-type [STh] and porcine-type [STp] variants), and colonization factors (CFs) among which CS6 is one of the most prevalent ETEC CFs. In this study we show that ETEC isolates expressing CS6+STh have higher copy numbers of the cssABCD operon encoding CS6 than those expressing CS6+STp. Long term cultivation of up to ten over-night passages of ETEC isolates harboring CS6+STh (n = 10) or CS6+STp (n = 15) showed instability of phenotypic expression of CS6 in a majority of the CS6+STp isolates, whereas most of the CS6+STh isolates retained CS6 expression. The observed instability was a correlated with loss of genes cssA and cssD as examined by PCR. Mobilization of the CS6 plasmid from an unstable CS6+STp isolate into a laboratory E. coli strain resulted in loss of the plasmid after a single over-night passage whereas the plasmid from an CS6+STh strain was retained in the laboratory strain during 10 passages. A sequence comparison between the CS6 plasmids from a stable and an unstable ETEC isolate revealed that genes necessary for plasmid stabilization, for example pemI, pemK, stbA, stbB and parM, were not present in the unstable ETEC isolate. Our results indicate that stable retention of CS6 may in part be affected by the stability of the plasmid on which both CS6 and STp or STh are located.