Widespread resistance to pyrethroids threatens malaria control in Africa. Consequently, several countries switched to carbamates and organophophates insecticides for indoor residual spraying. However, a mutation in the ace-1 gene conferring resistance to these compounds (ace-1R allele), is already present. Furthermore, a duplicated allele (ace-1D) recently appeared; characterizing its selective advantage is mandatory to evaluate the threat. Our data revealed that a unique duplication event, pairing a susceptible and a resistant copy of the ace-1 gene spread through West Africa. Further investigations revealed that, while ace-1D confers less resistance than ace-1R, the high fitness cost associated with ace-1R is almost completely suppressed by the duplication for all traits studied. ace-1 duplication thus represents a permanent heterozygote phenotype, selected, and thus spreading, due to the mosaic nature of mosquito control. It provides malaria mosquito with a new evolutionary path that could hamper resistance management.
number of X-autosome translocations have been described in the mouse, A which in the heterozygous female show a variegated phenotype for autosomal genes attached to the X chromosome ( CATTANACH 1961 ;RUSSELL and BANGHAM 1961 ; RUSSELL, BANGHAM and SAYLORS 1962). The primary cause in each instance was considered to be the inactivation of the associated autosomal genes (CATTA-NACH 1963;RUSSELL 1964) when the rearranged X is inactivated in the course of the normal process of X-inactivation (LYON 1961 ) . Evidence substantiating this hypothesis for one of the translocations has been obtained using both genetical and cytological tests (LYON 1963;OHNO and CATTANACH 1962).Several of the rearrangements have involved the translocation to the X of autosomal regions carrying more than one marker gene and here it has been shown that there is a secondary mechanism responsible for the variegation. Autosomal loci remote from the break point tend to be less influenced by the inactivation process than those lying closer to the break point (CATTANACH 1961;RUSSELL 1963), a phenomenon which appears to be analogous to the "spreading effect" observed in Drosophila V-type position effects (see review by LEWIS 1950) . Two clear mechanisms responsible for mouse translocation-induced variegation thus exist, (1 ) that due to the random inactivation of the rearranged and normal X in each cell, and (2) that caused by the Drosophila-type position effect which operates only when the rearranged X is in its inactive, heterochromatic condition. Variegation due to the second mechanism alone may be observed in situations where the randomness of X-inactivation is suppressed ( CATTANACH 1966a).We have recently been able to show that the position effect variegation is under genetic control (CATTANACH and ISAACSON 1965) ; genotypic selection for large and small amounts of albino areas in the coats of mice showing a translocationinduced variegation for albino was successful in establishing two lines of mice, one in which the autosomal (albino) locus was inactivated in every cell in which the rearranged X was inactivated. and another in which this was not always the case, i.e., the proportion of albino hairs was 50% in one line and 30% in the other. The data indicated that only one or a very few factors were responsible, and further investigations revealed that they were located in the rearranged X chromosome itself ( CATTANACH 1966b).
The mouse X-chromosome controlling elements, detected by their influence on the position effect variegation caused by the X-autosome translocation T (1; X) Ct, have been found to modify the heterozygous phenotypes of two X-linked genes. It is proposed that X-inactivation can be incomplete, the level of inactivation or the frequency of cells in which inactivation is incomplete being dependent upon the ‘state’ of the controlling element located in the X. The data suggest that this is a consequence of a reversal, or partial reversal, of inactivation of the X as a whole in some cells rather than a vairable spread of inactivation along the length of the X.
phoma Group. Use of arsenic trioxide in remission induction and consolidation therapy for acute promyelocytic leukaemia in the Australasian Leukaemia and Lymphoma Group (ALLG) APML4 study: a non-randomised phase 2 trial. Lancet Haematol. 2015;2(9):e357-e366. 7. Montesinos P, Bergua JM, Vellenga E, et al. Differentiation syndrome in patients with acute promyelocytic leukemia treated with all-trans retinoic acid and anthracycline chemotherapy: characteristics, outcome, and prognostic factors. Blood. 2009;113(4):775-783.
All therian mammals have a similar XY/XX sex-determination system except for a dozen species. The African pygmy mouse, Mus minutoides, harbors an unconventional system in which all males are XY, and there are three types of females: the usual XX but also XX * and X * Y ones (the asterisk designates a sex-reversal mutation on the X chromosome). The long-term evolution of such a system is a paradox, because X * Y females are expected to face high reproductive costs (e.g., meiotic disruption and loss of unviable YY embryos), which should prevent invasion and maintenance of a sex-reversal mutation. Hence, mechanisms for compensating for the costs could have evolved in M. minutoides. Data gathered from our laboratory colony revealed that X * Y females do compensate and even show enhanced reproductiveperformance in comparison to the XX and XX * ; they produce significantly more offspring due to (i) a higher probability of breeding, (ii) an earlier first litter, and (iii) a larger litter size, linked to (iv) a greater ovulation rate. These findings confirm that rare conditions are needed for an atypical sex-determination mechanism to evolve in mammals, and provide valuable insight into understanding modifications of systems with highly heteromorphic sex chromosomes. K E Y W O R D S :Breeding performance, life-history traits, sex chromosome evolution, sex-determination system, sex-reversed females, X * chromosome.
Coexistence often involves niche differentiation either as the result of environmental divergence, or in response to competition. Disentangling the causes of such divergence requires that environmental variation across space is taken into account, which is rarely done in empirical studies. We address the role of environmental variation versus competition in coexistence between two rodent species: Rhabdomys bechuanae (bechuanae) and Rhabdomys dilectus dilectus (dilectus) comparing their habitat preference and home range (HR) size in areas with similar climates, where their distributions abut (allopatry) or overlap (sympatry). Using Outlying Mean Index analyses, we test whether habitat characteristics of the species deviate significantly from a random sample of available habitats. In allopatry, results suggest habitat selection: dilectus preferring grasslands with little bare soil while bechuanae occurring in open shrublands. In sympatry, shrubland type habitats dominate and differences are less marked, yet dilectus selects habitats with more cover than bechuanae. Interestingly, bechuanae shows larger HRs than dilectus, and both species display larger HRs in sympatry. Further, HR overlaps between species are lower than expected. We discuss our results in light of data on the phylogeography of the genus and propose that evolution in allopatry resulted in adaptation leading to different habitat preferences, even at their distribution margins, a divergence expected to facilitate coexistence. However, since sympatry occurs in sites where environmental characteristics do not allow complete species separation, competition may explain reduced inter-species overlap and character displacement in HR size. This study reveals that both environmental variation and competition may shape species coexistence.
A supernumerary ''B-sex'' chromosome drives male sex determination in the Pachó n cavefish, Astyanax mexicanus Graphical abstract Highlights d Pachó n cavefish have supernumerary male-predominant B chromosomes (Bs) d This Pachó n B contain two loci of the putative gdf6b master sex-determining gene d gdf6b is only expressed in Pachó n male gonads and its knockout induces sex reversal d Pachó n B is a ''B-sex'' chromosome containing a putative male sex determination gene
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