Proliferation-driven mechanical compression induces signalling centre formation during mammalian organ development.

Localized sources of morphogens, called signalling centres, play a fundamental role in coordinating tissue growth and cell fate specification during organogenesis. However, how these signalling centres are established in tissues during embryonic development is still unclear. Here we show that the main signalling centre orchestrating development of rodent incisors, the enamel knot (EK), is specified by a cell proliferation-driven buildup in compressive stresses (mechanical pressure) in the tissue. Direct mechanical measurements indicate that the stresses generated by cell proliferation are resisted by the surrounding tissue, creating a circular pattern of mechanical anisotropy with a region of high compressive stress at its centre that becomes the EK. Pharmacological inhibition of proliferation reduces stresses and suppresses EK formation, and application of external pressure in proliferation-inhibited conditions rescues the formation of the EK. Mechanical information is relayed intracellularly through YAP protein localization, which is cytoplasmic in the region of compressive stress that establishes the EK and nuclear in the stretched anisotropic cells that resist the pressure buildup around the EK. Together, our data identify a new role for proliferation-driven mechanical compression in the specification of a model signalling centre during mammalian organ development.

Efecto de la ingestión de cultivo Saccharomyces cerevisiae y selenio en pollos de engorde expuestos a bajos niveles de aflatoxina B1 en la dieta / Effect of Saccharomyces cerevisiae Culture and Selenium Intake in Broiler Chickens Exposed to Low Levels of Aflatoxin B1 in the Ration

El presente estudio determinó el efecto de 0,1% de cultivo de levadura Saccharomyces cerevisiae (CSc) y 2 mg/kg de selenio (Se) sobre los índices productivos y concentración de proteínas totales en pollos de engorde que recibieron dietas con 0,07 mg/kg de aflatoxina B1 (AFB1). Un total de 480 pollos de engorde, de un día de nacidos, fueron asignados al azar para recibir 8 tipos de dietas durante 42 días. Se registró el peso de las aves (P), consumo de alimento (C), conversión de alimento (CV), ganancia de peso corporal (GPC), mortalidad (M) y a los 42 días se tomó suero sanguíneo de cada grupo para determinar la concentración de proteínas totales (PT). Las dietas correspondieron a los siguientes tratamientos (T) T1: grupo control que consiste en alimento comercial (AC) sin niveles detectables de aflatoxina; T2: AC + AFB1; T3: AC + CSc; T4: AC + AFB1 + CSc; T5: AC + Se; T6: AC + AFB1 + Se; T7: AC + CSc + Se; T8: AC + AFB1 + CSc + Se. La inclusión de CSc y/o Se en dietas con o sin AFB1 no alteró (P>0,05) el P, GPC, CV PT. El C incrementó (P£0,01) con la inclusión de CSc y/o Se en el alimento con AFB1 (T4, T6, T8), con respecto a los pollos que recibieron CSc y/o Se sin AFB1 (T3, T5, T7). La M en aves que recibieron AFB1 (T2, T4, T6, T7), incrementó (P<0,15), con respecto a las que recibieron dietas sin AFB1 (T1, T3, T5, T7). Estos resultados sugieren que la ingestión durante 42 días de 0,07 mg/kg de AFB1 en la dieta de pollos de engorde, puede tener efectos en algunos parámetros productivos, pudiendo aumentarse el consumo de alimento sin cambios en el P, GPC y CV por la inclusión individual o combinada de CSc y Se en las dietas contaminadas.

The present study determine the effect of 0.1% of yeast Saccharomyces cerevisiae (CSc) and 2 mg/kg de selenium (Se) over productive ranges and total protein concentrations on broiler chickens feed with a diet contaminated with 0.07 mg/kg of aflatoxin B1 (AFB1). 480 newborn broiler were randomly organized to receive 8 different diet during a 42 days period. Weight (P), Daily consume (C), Food convertion (CV) corporal weight gain (GPC), mortality (M) of broiler and at 42 days it was took blood serum of each group to determine total protein (PT) concentration. Diets corresponded the following treatments (T). T1: control group constitute by a commercial diet (AC) without any detectable level of aflatoxins; T2: AC + AFB1; T3: AC + CSc; T4: AC + AFB1 + CSc; T5: AC + Se; T6: AC + AFB1 + Se; T7: AC + CSc + Se; T8: AC + AFB1 + CSc + Se. The inclusion of CSc and/or Se diets with or without AFB1 did not affect (P>0.05) P, GPC, CV and PT. The increase of C (P£0.01) with inclusion of CSc and/or Se at feeding with AFB1 (T4, T6, T8), compared to boilers that received CSc and/or Se without AFB1 (T3, T5, T7). M on broilers that received AFB1 (T2, T4, T6, T8) incremented (P<0.15) compared to broilers that received a feeding without AFB1 (T1, T3, T5, T7). These results suggest that the ingestion during 42 days period with 0.07 mg/kg of AFB1 on diet of broiler, could have some effects on production parameters increasing consume of food without changes for P, GPC and CV by individual or combined inclusion of CSc and Se on contaminated diets.