A Pilot Study of Nulling in 22 Pulsars Using Mixture Modeling

The phenomenon of pulsar nulling, observed as the temporary inactivity of a pulsar, remains poorly understood both observationally and theoretically. Most observational studies that quantify nulling employ a variant of Ritchings (1976)'s algorithm which can suffer significant biases for pulsars where the emission is weak. Using a more robust mixture model method, we study pulsar nulling in a sample of 22 recently discovered pulsars, for which we publish the nulling fractions for the first time. These data clearly demonstrate biases of the former approach and show how an otherwise non-nulling pulsar can be classified as having significant nulls. We show that the population-wide studies that find a positive correlation of nulling with pulsar period/characteristic age can similarly be biased because of the bias in estimating the nulling fraction. We use our probabilistic approach to find the evidence for periodicity in the nulls in a subset of three pulsars in our sample. In addition, we also provide improved timing parameters for 17 of the 22 pulsars that had no prior follow-up.Comment: Accepted for publication in the Astrophysical Journal (ApJ

The chaperonin CCT8 facilitates spread of tobamovirus infection

The homeodomain transcription factor KNOTTED1 (KN1) functions in shoot meristem maintenance and is thought to move from cell to cell in a similar fashion as viral movement proteins. Both types of transported proteins bind to RNA, and associate with intercellular bridges formed by plasmodesmata. In a mutant screen for KN1 transport deficiency, a component of a type II chaperonin complex, CCT8, was identified, and found to interact with non-cell-autonomous proteins. The cct8 mutants are characterized by limited functionality of non-cell-autonomous proteins after their movement, and a phenotype resembling lack of homeodomain protein activity. Evidence suggests that CCT8 functions in post-translocational refolding of transported proteins. Here we show that spread of tobamovirus infection is reduced in a cct8 mutant. This suggests that similar to KN1, viral movement proteins are unfolded and refolded during transport to gain functionality in the receiving cells

Plasmodesmata: Channels for Viruses on the Move

The symplastic communication network established by plasmodesmata (PD) and connected phloem provides an essential pathway for spatiotemporal intercellular signaling in plant development but is also exploited by viruses for moving their genomes between cells in order to infect plants systemically. Virus movement depends on virus-encoded movement proteins (MPs) that target PD and therefore represent important keys to the cellular mechanisms underlying the intercellular trafficking of viruses and other macromolecules. Viruses and their MPs have evolved different mechanisms for intracellular transport and interaction with PD. Some viruses move from cell to cell by interacting with cellular mechanisms that control the size exclusion limit of PD whereas other viruses alter the PD architecture through assembly of specialized transport structures within the channel. Some viruses move between cells in the form of assembled virus particles whereas other viruses may interact with nucleic acid transport mechanisms to move their genomes in a non-encapsidated form. Moreover, whereas several viruses rely on the secretory pathway to target PD, other viruses interact with the cortical endoplasmic reticulum and associated cytoskeleton to spread infection. This chapter provides an introduction into viruses and their role in studying the diverse cellular mechanisms involved in intercellular PD-mediated macromolecular trafficking