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Mackenzie, K.

Publications and source records attributed to Mackenzie, K..

2 recordsLinked to original sources

Diversity of the woodland strawberry inflorescences results from heterochrony antagonistically regulated by FvTFL1 and FvFT1

A vast variety of inflorescence architectures have formed during angiosperm evolution. Here we analyze the diversity and development of the woodland strawberry inflorescence. We show that it is a thyrse: a compound inflorescence in which the primary monopodial axis supports lateral sympodial branches, thus combining features of racemes and cymes. We demonstrate that this architecture is related to differences in the size and shape of the primary and lateral inflorescence meristems. We further show that woodland strawberry homologs of TERMINAL FLOWER 1 (TFL1) and FLOWERING LOCUS T (FT) antagonistically regulate the development of both the racemose and cymose components of the strawberry thyrse: the loss of functional FvTFL1 and overexpression of FvFT1 reduce the number and complexity of the cymose components, whereas silencing of FvFT1 has the opposite effect and can partially rescue the fvtfl1 mutation. We complement our experimental findings with a computational model, which captures the development of the woodland strawberry inflorescence using a small set of rules, and shows that its phenotypic diversity can be explained in terms of heterochrony resulting from the opposite action of FvTFL1 and FvFT1 on the progression from the branching to flowering state.

plant biology↗

Enhanced post-traumatic headache-like behaviors and diminished contribution of peripheral CGRP in female rats following a mild closed head injury

IntroductionFemales are thought to have increased risk of developing posttraumatic headache (PTH) following a traumatic head injury, or concussion. However, the processes underlying this susceptibility remain unclear. We previously explored the development of PTH-like pain behaviors in a novel rat model of mild closed head injury, along with the ability of sumatriptan and an anti-calcitonin-gene-related peptide monoclonal antibody to ameliorate these behaviors. Here, we explored the development of PTH-like behaviors and the effectiveness of these headache therapies in females subjected to the same head trauma protocol. MethodsAdult female Sprague Dawley rats were subjected to a mild closed head injury using a weight-drop device. Characterization of headache and pain related behaviors included assessment of changes in cutaneous cephalic and extracephalic tactile pain sensitivity, using von Frey monofilaments. Sensitivity to headache/migraine triggers was tested by examining the effect of systemic administration of a low-dose of glyceryl trinitrate (GTN). Treatments included acute systemic administration of sumatriptan and repeated systemic administration of a mouse anti-calcitonin-gene-related peptide monoclonal antibody. Serum levels of calcitonin-gene-related peptide were measured at various time points in females and males after the head injury. ResultsFemale rats subjected to a mild closed head injury developed cutaneous mechanical hyperalgesia, that was limited to the cephalic region, and was resolved 4 weeks later. Cephalic pain hypersensitivity was ameliorated by treatment with sumatriptan, but was resistant to an early and prolonged treatment with the anti-CGRP monoclonal antibody. Following the resolution of the head injury-evoked cephalic hypersensitivity, administration of GTN produced a renewed and pronounced cephalic and extracephalic pain hypersensitivity that was inhibited by sumatriptan, but only partially by the anti-CGRP treatment. CGRP serum levels were elevated in females but not in males at 7 days post head injury. ConclusionsDevelopment of PTH-like pain behaviors following a mild closed head injury, and responsiveness to treatment in rats is sexually dimorphic. When compared to males, female rats display a prolonged state of cephalic hyperalgesia, increased responsiveness to a headache trigger, and a poorer effectiveness of an early and prolonged anti-CGRP treatment. The increased risk of females to develop PTH may be linked to enhanced responsiveness of peripheral and/or central pain pathways and a mechanism independent of peripheral CGRP signaling.

neuroscience↗