Many mammals grow up with siblings, and interactions between them can influence offspring phenotype and fitness. Among these interactions, sibling competition between different-age offspring should lead to reproductive and survival costs on the younger sibling, while sibling cooperation should improve younger sibling's reproductive potential and survival. However, little is known about the consequences of sibling effects on younger offspring life-history trajectory, especially in long-lived mammals. We take advantage of a large, multigenerational demographic dataset from semi-captive Asian elephants to investigate how the presence and sex of elder siblings influence the sex, survival until 5 years old, body condition, reproductive success (i.e. age at first reproduction and lifetime reproductive success) and long-term survival of subsequent offspring. We find that elder siblings have heterogeneous effects on subsequent offspring life-history traits depending on their presence, their sex and the sex of the subsequent offspring (named focal calf). Overall, the presence of an elder sibling (either sex) strongly increased focal calf long-term survival (either sex) compared to sibling absence. However, elder sisters had higher impact on the focal sibling than elder brothers. Focal females born after a female display higher long-term survival, and decreased age at first reproduction when raised together with an elder sister rather than a brother. Focal males born after a female rather than a male showed lower survival but higher body weight when both were raised together. We did not detect any sibling effects on the sex of the focal calf sex, survival until 5 years old and lifetime reproductive success. Our results highlight the general complexity of sibling effects, but broadly that elder siblings can influence the life-history trajectory of subsequent offspring. We also stress the importance of considering all life stages when evaluating sibling effects on life trajectories.
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http://dx.doi.org/10.1111/1365-2656.13573 | DOI Listing |
Genes (Basel)
November 2024
Department of Neuroscience, IRCCS Stella Maris Foundation, 56128 Pisa, Italy.
Background: Autosomal recessive inherited pathogenetic variants in the histidine triad nucleotide-binding protein 1 () gene are responsible for an axonal Charcot-Marie-Tooth neuropathy associated with neuromyotonia, a phenomenon resulting from peripheral nerve hyperexcitability that causes a spontaneous muscle activity such as persistent muscle contraction, impaired relaxation and myokymias.
Methods: Herein, we describe two brothers in whom biallelic variants were identified following a multidisciplinary approach.
Results: The younger brother came to our attention for clinical evaluation of moderate intellectual disability, language developmental delay, and some behavioral issues.
Craniosynostosis (CS) is the premature fusion of skull sutures, with all sutures except the metopic suture typically fusing in adulthood. Premature fusion constrains brain growth, leading to abnormal skull shape and potential neurocognitive or neurological issues, along with syndromic features in some cases. While CS is rare, its occurrence in siblings is exceptionally uncommon and holds significant academic importance.
View Article and Find Full Text PDFAnn Hum Genet
November 2024
Division of Genetics, Narayana Hrudayalaya Hospitals/Mazumdar-Shaw Medical, Centre, Bangalore, Karnataka, India.
Introduction: Combined oxidative phosphorylation (OXPHOS) deficiency 44 (COXPD44; MIM# 618855) is caused by biallelic pathogenic variants in FAS-activated serine-threonine kinase domain 2 (FASTKD2) (MIM# 612322). COXPD44 is characterized by variable clinical features-developmental delay, chronic epileptic encephalopathy, seizure disorder/status epilepticus and cerebellar ataxia. We ascertained one sib with episodic acute encephalomyopathy triggered by acute gastroenteritis and associated with haematological abnormalities, rhabdomyolysis leading to acute kidney injury, hypotensive shock leading to early death and a similarly affected sib with early death.
View Article and Find Full Text PDFTher Adv Rare Dis
October 2024
Department of Otorhinolaryngology & HNS, Leiden University Medical Centre, Leiden, The Netherlands.
Here, we describe two congenitally deaf male siblings with the same compound heterozygotic, likely pathogenic mutations in the FGF3 gene, associated with the labyrinthine aplasia, microtia and microdontia (LAMM) syndrome. Both children had bilateral cochleovestibular aplasia, precluding cochlear implantation. The elder brother received an auditory brainstem implant (ABI) with very limited auditory responses.
View Article and Find Full Text PDFFront Pediatr
September 2024
Department of Respiratory Medicine, Beijing Children's Hospital, National Center for Children's Health, Capital Medical University, Beijing, China.
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