Sinorhizobium meliloti Phage ΦM9 Defines a New Group of T4 Superfamily Phages with Unusual Genomic Features but a Common T=16 Capsid.

UNLABELLED: Relatively little is known about the phages that infect agriculturally important nitrogen-fixing rhizobial bacteria. Here we report the genome and cryo-electron microscopy structure of the Sinorhizobium meliloti-infecting T4 superfamily phage ΦM9. This phage and its close relative Rhizobium phage vB_RleM_P10VF define a new group of T4 superfamily phages. These phages are distinctly different from the recently characterized cyanophage-like S. meliloti phages of the ΦM12 group. Structurally, ΦM9 has a T=16 capsid formed from repeating units of an extended gp23-like subunit that assemble through interactions between one subunit and the adjacent E-loop insertion domain. Though genetically very distant from the cyanophages, the ΦM9 capsid closely resembles that of the T4 superfamily cyanophage Syn9. ΦM9 also has the same T=16 capsid architecture as the very distant phage SPO1 and the herpesviruses. Despite their overall lack of similarity at the genomic and structural levels, ΦM9 and S. meliloti phage ΦM12 have a small number of open reading frames in common that appear to encode structural proteins involved in interaction with the host and which may have been acquired by horizontal transfer. These proteins are predicted to encode tail baseplate proteins, tail fibers, tail fiber assembly proteins, and glycanases that cleave host exopolysaccharide. IMPORTANCE: Despite recent advances in the phylogenetic and structural characterization of bacteriophages, only a small number of phages of plant-symbiotic nitrogen-fixing soil bacteria have been studied at the molecular level. The effects of phage predation upon beneficial bacteria that promote plant growth remain poorly characterized. First steps in understanding these soil bacterium-phage dynamics are genetic, molecular, and structural characterizations of these groups of phages. The T4 superfamily phages are among the most complex phages; they have large genomes packaged within an icosahedral head and a long, contractile tail through which the DNA is delivered to host cells. This phylogenetic and structural study of S. meliloti-infecting T4 superfamily phage ΦM9 provides new insight into the diversity of this family. The comparison of structure-related genes in both ΦM9 and S. meliloti-infecting T4 superfamily phage ΦM12, which comes from a completely different lineage of these phages, allows the identification of host infection-related factors.

True abdominal epilepsy is clonic jerking of the abdominal musculature.

Abdominal epilepsy (AE) has long been reported as a rare phenomenon in children with various episodic gastrointestinal sensory and painful symptoms suspected to be due to epileptic seizures. Originally, AE was diagnosed when abdominal sensory or painful symptoms were associated with pain, temporal lobe origin, an epileptiform or paroxysmal EEG pattern, and a clinical response to antiseizure medication. AE has also been associated with non-epileptic etiologies such as migraine. Reports of abdominal epilepsy based on an abnormal EEG or clinical response to antiseizure medication without diagnosis confirmation by video-EEG are at best speculative, and at worst, misdiagnoses. We describe three adult patients with focal aware motor seizures manifesting as recurrent, isolated prolonged painless rhythmic clonic jerking of the abdominal musculature including epilepsia partialis continua. All patients had a contralateral structural lesion on high-resolution brain MRI in the abdominal region of the motor homunculus. Standard EEG was unrevealing and only after extra EEG electrodes and video-EEG monitoring was the ictal origin confirmed. Historically, AE has been described as a disorder involving subjective sensory symptoms including vague abdominal pain, instead of epileptic motor signs of abdominal clonic jerking. We recommend replacing the use of vague terms such as AE with International League Against Epilepsy terminology along with diagnostic confirmation validated by video-EEG monitoring. [Published with video sequence].