RESUMEN
Collecting lymphatic vessels (cLVs) exhibit spontaneous contractions with a pressure-dependent frequency, but the identity of the lymphatic pacemaker cell is still debated. By analogy to pacemakers in the GI and lower urinary tracts, proposed cLV pacemaker cells include interstitial cells of Cajal like cells (ICLC), pericytes, as well as the lymphatic muscle (LMCs) cells themselves. Here we tested the extent to which these cell types are invested into the mouse cLV wall and if any cell type exhibited morphological and functional processes characteristic of pacemaker cells: a contiguous network; spontaneous Ca2+ transients; and depolarization-induced propagated contractions. We employed inducible Cre (iCre) mouse models routinely used to target these specific cell populations including: c-kitCreERT2 to target ICLC; PdgfrßCreERT2 to target pericytes; PdgfrαCreER™ to target CD34+ adventitial fibroblast-like cells or ICLC; and Myh11CreERT2 to target LMCs. These specific inducible Cre lines were crossed to the fluorescent reporter ROSA26mT/mG, the genetically encoded Ca2+ sensor GCaMP6f, and the light-activated cation channel rhodopsin2 (ChR2). c-KitCreERT2 labeled both a sparse population of LECs and round adventitial cells that responded to the mast cell activator compound 48-80. PdgfrßCreERT2 drove recombination in both adventitial cells and LMCs, limiting its power to discriminate a pericyte specific population. PdgfrαCreER™ labeled a large population of interconnected, oak leaf-shaped cells primarily along the adventitial surface of the vessel. Titrated induction of the smooth muscle-specific Myh11CreERT2 revealed a LMC population with heterogeneous morphology. Only LMCs consistently, but heterogeneously, displayed spontaneous Ca2+ events during the diastolic period of the contraction cycle, and whose frequency was modulated in a pressure-dependent manner. Optogenetic depolarization through the expression of ChR2 by Myh11CreERT2, but not PdgfrαCreER™ or c-KitCreERT2, resulted in a propagated contraction. These findings support the conclusion that LMCs, or a subset of LMCs, are responsible for mouse cLV pacemaking.
RESUMEN
The genetic architecture underlying resistance in maize to southern leaf blight (SLB) caused by Cochliobolus heterostrophus race O is not well understood. The objective of this study was to identify loci contributing to SLB resistance in two recombinant inbred line populations and to compare these to SLB resistance loci in other populations. The two populations used were derived from crosses between maize inbred lines H99 and B73 (HB population-142 lines) and between B73 and B52 (BB population-186 lines). They were evaluated for SLB resistance and for days from planting to anthesis (DTA) in 2005 and 2006. Two replications arranged as randomized complete blocks were assessed in each year for each population. Entry mean heritabilities for disease resistance were high for both populations (0.876 and 0.761, respectively). Quantitative trait loci (QTL) for SLB resistance were identified in bins 3.04 (two QTL), 6.01, and 8.05 in the HB population and in bin 2.07 in the BB population. No overlap of DTA and SLB resistance QTL was observed, nor was there any phenotypic correlation between the traits. A comparison of the results of all published SLB resistance QTL studies suggested that bins 3.04 and 6.01 are 'hotspots' for SLB resistance QTL.
