Results on FF-continuous graphs

summary:For any nontrivial connected graph $F$ and any graph $G$, the {\it $F$-degree} of a vertex $v$ in $G$ is the number of copies of $F$ in $G$ containing $v$. $G$ is called {\it $F$-continuous} if and only if the $F$-degrees of any two adjacent vertices in $G$ differ by at most 1; $G$ is {\it $F$-regular} if the $F$-degrees of all vertices in $G$ are the same. This paper classifies all $P_4$-continuous graphs with girth greater than 3. We show that for any nontrivial connected graph $F$ other than the star $K_{1,k}$, $k \geq 1$, there exists a regular graph that is not $F$-continuous. If $F$ is 2-connected, then there exists a regular $F$-continuous graph that is not $F$-regular

An Orthogonal Proteomic Screen of Zika virus Reveals Specific Targeting of Neuronal Differentiation Factors

Zika virus (ZIKV) has recently emerged as a global health concern owing to its widespread diffusion and its association with severe neurological symptoms and microcephaly in newborns1. However, the molecular mechanisms that are responsible for the pathogenicity of ZIKV remain largely unknown. Here we use human neural progenitor cells and the neuronal cell line SK-N-BE2 in an integrated proteomics approach to characterize the cellular responses to viral infection at the proteome and phosphoproteome level, and use affinity proteomics to identify cellular targets of ZIKV proteins. Using this approach, we identify 386 ZIKV-interacting proteins, ZIKV-specific and pan-flaviviral activities as well as host factors with known functions in neuronal development, retinal defects and infertility. Moreover, our analysis identified 1,216 phosphorylation sites that are specifically up- or downregulated after ZIKV infection, indicating profound modulation of fundamental signalling pathways such as AKT, MAPK-ERK and ATM-ATR and thereby providing mechanistic insights into the proliferation arrest elicited by ZIKV infection. Functionally, our integrative study identifies ZIKV host-dependency factors and provides a comprehensive framework for a system-level understanding of ZIKV-induced perturbations at the levels of proteins and cellular pathways